Effects of Yishentongluo recipe on Nrf2 and HO-1 pathway activation leading to reduction of oxidative stress and kidney fibrosis in membranous nephropathy rat model / Efectos de la receta de Yishentongluo sobre la activación de las vías Nrf2 y HO-1 que conducen a la reducción del estrés oxidativo y fibrosis renal en un modelo de rata con nefropatía membranosa

This study investigated Yishentongluo Recipe (YSTLF) effects on renal oxidative stress and fibrosis in membranous nephropathy (MN) rats. MN was induced by cationized bovine serum albumin injection. Rats were divided into control, MN, YSTLF, and benazepril groups. After four weeks of treatment, urine protein levels (UTP), serum total cholesterol (TC), triglycerides (TG), total protein (TP), and albumin (ALB) were assessed. Kidney microstructure, IgG immune complex deposition, and protein expressions of superoxide dismutase (SOD), malondialdehyde (MDA), transforming growth factor ß1 (TGF-ß1), collagen I (Collagen-I), α-smooth muscle actin (α-SMA), nuclear factor E2-related factor (Nrf2), haem oxygenase 1 (HO-1), and NADPH oxidase 4 (NOX4) were evaluated. YSTLF and BNPL treatments reduced UTP, TC, TG, increased TP and ALB levels, downregulated TGF-ß1, Collagen-I, and α-SMA, and upregulated Nrf2, HO-1, and NOX4. YSTLF partially reversed SOD reduction and MDA elevation, suggesting its efficacy in alleviating renal oxidative stress and fibrosis in MN rats via Nrf2/HO-1 signaling pathway activation.

Este estudio investigó los efectos de la receta Yishentongluo (YSTLF) sobre el estrés oxidativo renal y la fibrosis en ratas con nefropatía membranosa (MN). La MN se indujo mediante inyección de albúmina sérica bovina cationizada. Las ratas se dividieron en grupos de control, MN, YSTLF y benazepril. Después de cuatro semanas de tratamiento, se evaluaron los niveles de proteína en orina (UTP), colesterol total (CT), triglicéridos (TG), proteína total (TP) y albúmina (ALB) en suero. Se evaluaron la microestructura renal, el depósito de complejos inmunes IgG y expresiones proteicas de superóxido dismutasa (SOD), malondialdehído (MDA), factor de crecimiento transformante ß1 (TGF-ß1), colágeno I (Colágeno-I), α-actina del músculo liso (α-SMA), el factor nuclear E2 (Nrf2), la hemooxigenasa 1 (HO-1) y la NADPH oxidasa 4 (NOX4). Los tratamientos con YSTLF y BNPL redujeron UTP, TC, TG, aumentaron los niveles de TP y ALB, regularon negativamente TGF-ß1, Colágeno-I y α-SMA, y regularon positivamente Nrf2, HO-1 y NOX4. YSTLF revirtió parcialmente la reducción de SOD y la elevación de MDA, lo que sugiere su eficacia para aliviar el estrés oxidativo renal y la fibrosis en ratas MN mediante la activación de la vía de señalización Nrf2/HO-1.

Impact of Aging on the Morphology of the Adrenal Gland in Rats / Impacto del Envejecimiento en la Morfología de la Glándula Suprarrenal en Ratas

SUMMARY: Aging is an inevitable biological process that affects the function of all organs, including the adrenal gland, which is essential for producing steroid hormones that regulate metabolism, stress response, and immune activation. Understanding how aging affects the morphology of this gland is crucial to developing interventions to mitigate its adverse effects. Thus, this study aimed to describe the morphoquantitative alterations of the adrenal gland in senescent Sprague Dawley rats compared to adult rats. Twelve male rats were divided into 6 adult rats aged 6 months (group A) and 6 senescent rats aged 36 months (group S). Histopathological studies, quantification of collagen fibers types I and III, and stereological analysis were performed to determine the volume density (Vv), surface area (Sv), and number (Nv) of the nuclei of the zona fasciculata cells. Adrenal gland tissue from group S presented dysplasia, metaplasia, intracellular fat accumulation, fibrosis, blood vessel dilation, and increased presence of apoptotic cells. Capsule thickening and increased collagen type I were also observed. There was a significant decrease in Vv, Sv, and Nv of zona fasciculata nuclei in group S compared to group A. The results indicate that aging induces significant morphoquantitative changes in the adrenal gland, which could contribute to the decrease in glucocorticoid production and alterations in aldosterone and cortisol secretion observed in senescence. Understanding these alterations is crucial to developing interventions that mitigate the adverse effects of aging on the endocrine system.

El envejecimiento es un proceso biológico inevitable que afecta la función de todos los órganos, incluida la glándula suprarrenal, fundamental para la producción de hormonas esteroides que regulan el metabolismo, la respuesta al estrés y la activación inmunológica. Comprender cómo el envejecimiento afecta la morfología de esta glándula es crucial para desarrollar intervenciones que mitiguen sus efectos adversos. Así, el objetivo de este estudio fue describir las alteraciones morfocuantitativas de la glándula suprarrenal en ratas Sprague Dawley senescentes comparadas con ratas adultas. Se utilizaron 12 ratas macho, divididas en dos grupos: 6 ratas adultas de 6 meses de edad (grupo A) y 6 ratas senescentes de 36 meses de edad (grupo S). Se realizaron estudios histopatológicos, cuantificación de fibras de colágeno tipos I y III y análisis estereológicos para determinar la densidad de volumen (Vv), de superficie (Sv) y de número (Nv) de los núcleos de las células de la zona fasciculada. El tejido de la glándula suprarrenal del grupo S presentó displasia, metaplasia, acumulación de grasa intracelular, fibrosis, dilatación de vasos sanguíneos y mayor presencia de células apoptósicas. También se observó un engrosamiento de la cápsula y un incremento del colágeno tipo I. Hubo una disminución significativa en Vv, Sv y Nv de los núcleos de la zona fasciculada en el grupo S en comparación con el grupo A. Los resultados indican que el envejecimiento induce cambios morfocuantitativos significativos en la glándula suprarrenal, lo que podría contribuir a la disminución en la producción de glucocorticoides y alteraciones en la secreción de aldosterona y cortisol observadas en la senescencia. Comprender estas alteraciones es crucial para desarrollar intervenciones que mitiguen los efectos adversos del envejecimiento en el sistema endocrino.

Guttate Morphea in a 31-year-old Filipino female: A diagnostic challenge in its early stage

Introduction@#Morpheq, also known as localized scleroderma, describes a distinctive inflammatory skin disorder that ultimately leads to sclerosis. It is differentiated from systemic scleroderma by the absence of vasculopathy and organ involvement. Initial erythema may precede the sclerotic stage by a few months causing initial diagnostic confusion. High index of suspicion and knowledge of disease evolution are essential. We report a case of morphea and its progression, the diagnostic approach and the importance of early treatment and long-term monitoring. @*Case Summary@#A 3l-year-old Filipino female who presented with multiple erythematous plagues on the trunk and extremities and arthralgia was initially diagnosed with cutaneous drug reaction. Prompt treatment led to partial relief of symptoms. However, two months later, eruption of multiple ivory-white small patches and plaques were noted on the same affected areas prompting an impression of morphea. Serum markers revealed elevated antinuclear antibody levels and negative anti-Scl70/anti-centromere serum autoantibodies. Skin biopsy showed homogenized thick dermal collagen bundles confirming the diagnosis of morphea. Topical therapy with calcipotriol + betamethasone dipropionate ointment showed remarkable improvement with decrease in erythema and softening of the lesions while adjunct narrowband-UVB phototherapy also provided relief due to its ability to reduce collagen synthesis and cytokine production. @*Conclusion@#Morphea may be easily misdiagnosed during the early stages especially if sclerosis ensues late in the disease. Characteristic clinical appearance of erythematous plaques with violaceous borders may not always be present. Histologic examination and serum autoantibodies help exclude other disorders with the same clinical and histopathological spectrum. Treatment is individualized depending on the severity and depth of skin involvement, early treatment and monitoring should be initiated before complications arise.

Exosomes derived from miR-133a-3p engineered mesenchymal stem cells promote myocardial repair in rats after acute myocardial infarction / 中华心血管病杂志

Objective: To investigate the effects of exosome derived from miR-133a-3p engineered human umbilical cord blood mesenchymal stem cells (ucMSC) on myocardial repair after acute myocardial infarction (AMI) in rats. Methods: UcMSC was amplified and cultured in vitro. Lentiviral carrying miR-133a-3p and negative control vectors were transfected into ucMSC. Exosomes secreted by the transfected ucMSC were named miR-133a-3p-Exo and miR-NC-Exo, respectively. The AMI model of rats was established by ligation of the left anterior descending coronary artery. MiR-133a-3p-Exo or miR-NC-Exo were then injected into the border zone of the infarct area. Cardiac function was assessed by echocardiography after twenty-eight days of intervention, and Masson staining was used to evaluate the area of myocardial fibrosis post-AMI. The myocardial apoptosis after infarction was evaluated by TUNEL staining and the angiogenesis after infarction was evaluated by immunofluorescence staining in the current study. Results: Compared with the miR-NC-Exo group, the left ventricular ejection fraction in the miR-133a-3p-Exo group was significantly increased ((47.4%±9.8%) vs. (64.2%±8.9%), P<0.05). While the myocardial fibrosis area ((31.2%±7.3%) vs. (18.0%±1.5%), P<0.01) and the percentage of apoptotic cardiomyocytes ((25.6%±3.6%) vs. (15.1%±4.4%), P<0.05) was significantly reduced in the miR-133a-Exo group. Besides, the expression of CD31 and α-smooth muscle actin (α-SMA) were also increased significantly in the miR-133a-3p-Exo group compared to the miR-NC-Exo group (CD31: (2.9±0.9) vs. (13.9±2.0), P<0.000 1, α-SMA: (3.5±0.9) vs. (11.0±1.6), P<0.000 1). Conclusion: Exosome derived from miR-133a-3p engineered ucMSC effectively inhibited myocardial apoptosis and promoted angiogenesis, thus improving the cardiac function after myocardial infarction in rats.

Exosomes derived from miR-133a-3p engineered mesenchymal stem cells promote myocardial repair in rats after acute myocardial infarction / 中华心血管病杂志

Objective: To investigate the effects of exosome derived from miR-133a-3p engineered human umbilical cord blood mesenchymal stem cells (ucMSC) on myocardial repair after acute myocardial infarction (AMI) in rats. Methods: UcMSC was amplified and cultured in vitro. Lentiviral carrying miR-133a-3p and negative control vectors were transfected into ucMSC. Exosomes secreted by the transfected ucMSC were named miR-133a-3p-Exo and miR-NC-Exo, respectively. The AMI model of rats was established by ligation of the left anterior descending coronary artery. MiR-133a-3p-Exo or miR-NC-Exo were then injected into the border zone of the infarct area. Cardiac function was assessed by echocardiography after twenty-eight days of intervention, and Masson staining was used to evaluate the area of myocardial fibrosis post-AMI. The myocardial apoptosis after infarction was evaluated by TUNEL staining and the angiogenesis after infarction was evaluated by immunofluorescence staining in the current study. Results: Compared with the miR-NC-Exo group, the left ventricular ejection fraction in the miR-133a-3p-Exo group was significantly increased ((47.4%±9.8%) vs. (64.2%±8.9%), P<0.05). While the myocardial fibrosis area ((31.2%±7.3%) vs. (18.0%±1.5%), P<0.01) and the percentage of apoptotic cardiomyocytes ((25.6%±3.6%) vs. (15.1%±4.4%), P<0.05) was significantly reduced in the miR-133a-Exo group. Besides, the expression of CD31 and α-smooth muscle actin (α-SMA) were also increased significantly in the miR-133a-3p-Exo group compared to the miR-NC-Exo group (CD31: (2.9±0.9) vs. (13.9±2.0), P<0.000 1, α-SMA: (3.5±0.9) vs. (11.0±1.6), P<0.000 1). Conclusion: Exosome derived from miR-133a-3p engineered ucMSC effectively inhibited myocardial apoptosis and promoted angiogenesis, thus improving the cardiac function after myocardial infarction in rats.

Chemical characterization and effects of volatile oil of Alpinia zerumbet on the quality of collagen deposition and caveolin-1 expression in a muscular fibrosis murine model / Caracterização química e efeitos do óleo volátil de Alpinia zerumbet na qualidade da deposição do colágeno e expressão da caveolina-1 em modelo murino de fibrose muscular

Abstract This study evaluated the effect of the volatile oil of Alpinia zerumbet (VOAz) on caveolin-1 gene expression and muscular fibrosis. The rats were immobilized to induce fibrosis of the gastrocnemius muscle, and they were treated with VOAz. Collagen quality was assessed by histology and the expression of the caveolin-1 (CAV-1) gene was evaluated using qPCR. Histomorphological analysis indicated a significant reduction in the perimeter, width, and intensity of collagen in the treated groups, thus showing that the oil was effective in regulating the quality of collagen at the three concentrations. The results of expression levels suggested a decrease in the lesioned group and in two treatment groups (0.0115 µg/g and 0.009 µg/g). However, with the lowest concentration (0.0065 µg/g), no significant difference was observed, with levels similar to those found in healthy tissue. Therefore, the results showed that VOAz has the potential to be a non-invasive and low-cost alternative to aid in the treatment of muscular fibrosis.

Resumo Este estudo avaliou o efeito do óleo volátil de Alpinia zerumbet (OVAz) na expressão do gene da caveolina-1 e na fibrose muscular. Os ratos foram imobilizados para induzir a fibrose do músculo gastrocnêmio, e foram tratados com OVAz. A qualidade do colágeno foi avaliada com histologia e à expressão do gene caveolina-1 (CAV-1) foi avaliada usando qPCR. A análise histomorfológica indicou uma redução significativa no perímetro, largura e intensidade do colágeno nos grupos tratados. Os resultados dos níveis de expressão sugeriram diminuição nos grupos de lesão e em dois grupos de tratamento (0,0115 µg/g e 0,009 µg/g). No entanto, com a menor concentração (0,0065 µg/g), não foi observada diferença significativa, apresentando níveis semelhantes aos encontrados em tecido saudável. O uso do OVAz foi eficaz para reverter as alterações do colágeno causadas pela fibrose, e sua menor concentração apresentou uma possível tendência de aumento na expressão do CAV-1. Portanto, os resultados mostraram que o OVAz tem potencial para ser uma alternativa não invasiva e de baixo custo para auxiliar no tratamento da fibrose muscular.

Endometrial mesenchymal stromal/stem cells improve regeneration of injured endometrium in mice

BACKGROUND: The monthly regeneration of human endometrial tissue is maintained by the presence of human endometrial mesenchymal stromal/stem cells (eMSC), a cell population co-expressing the perivascular markers CD140b and CD146. Endometrial regeneration is impaired in the presence of intrauterine adhesions, leading to infertility, recurrent pregnancy loss and placental abnormalities. Several types of somatic stem cells have been used to repair the damaged endometrium in animal models, reporting successful pregnancy. However, the ability of endometrial stem cells to repair the damaged endometrium remains unknown. METHODS: Electrocoagulation was applied to the left uterine horn of NOD/SCID mice causing endometrial injury. Human eMSC or PBS was then injected into the left injured horn while the right normal horn served as controls. Mice were sacrificed at different timepoints (Day 3, 7 and 14) and the endometrial morphological changes as well as the degree of endometrial injury and repair were observed by histological staining. Gene expression of various inflammatory markers was assessed using qPCR. The functionality of the repaired endometrium was evaluated by fertility test. RESULTS: Human eMSC successfully incorporated into the injured uterine horn, which displayed significant morphological restoration. Also, endometrium in the eMSC group showed better cell proliferation and glands formation than the PBS group. Although the number of blood vessels were similar between the two groups, gene expression of VEGF-α significantly increased in the eMSC group. Moreover, eMSC had a positive impact on the regeneration of both stromal and epithelial components of the mouse endometrium, indicated by significantly higher vimentin and CK19 protein expression. Reduced endometrial fibrosis and down-regulation of fibrosis markers were also observed in the eMSC group. The eMSC group had a significantly higher gene expression of anti-inflammatory factor Il-10 and lower mRNA level of pro-inflammatory factors Ifng and Il-2, indicating the role of eMSC in regulation of inflammatory reactions. The eMSC group showed higher implantation sites than the PBS group, suggesting better endometrial receptivity with the presence of newly emerged endometrial lining. CONCLUSIONS: Our findings suggest eMSC improves regeneration of injured endometrium in mice.

Therapeutic potential of stem cell and melatonin on the reduction of CCl4-induced liver fibrosis in experimental mice model / Potencial terapêutico de células-tronco e melatonina na redução da fibrose hepática induzida por CCl4 no modelo de ratos experimentais

Liver fibrosis is initial stage of any chronic liver disease and its end stage is develops into cirrhosis. Chronic liver diseases are a crucial global health issue and the cause of approximately 2 million deaths per year worldwide. Cirrhosis is currently the 11th most common cause of death globally. Mesenchymal stem cell (MSCs) treatment is the best way to treat acute and chronic liver disease. The aim of this study is to improve the therapeutic potential of MSCs combined with melatonin (MLT) to overcome CCl4-induced liver fibrosis and also investigate the individual impact of melatonin and MSCs against CCl4-induced liver impairment in animal model. Female BALB/c mice were used as CCL4-induced liver fibrotic animal model. Five groups of animal model were made; negative control, Positive control, CCl4+MSCs treated group, CCl4+MLT treated group and CCl4+MSCs+MLT treated group. Cultured MSCs from mice bone marrow were transplanted to CCl4-induced liver injured mice model, individually as well as together with melatonin. Two weeks after MSCs and MLT administration, all groups of mice were sacrificed for examination. Morphological and Histopathological results showed that combined therapy of MSCs+MLT showed substantial beneficial impact on CCl4-induced liver injured model, compared with MSCs and MLT individually. Biochemically, considerable reduction was observed in serum bilirubin and ALT levels of MLT+MSC treated mice, compared to other groups. PCR results shown down-regulation of Bax and up-regulation of Bcl-xl and Albumin, confirm a significant therapeutic effect of MSCs+MLT on CCI4-induced liver fibrosis. From the results, it is concluded that combined therapy of MSCs and MLT show strong therapeutic effect on CCL4-induced liver fibrosis, compared with MSCs and MLT individually.

A fibrose hepática é a fase inicial de qualquer doença hepática crônica, e em sua fase final desenvolve-se para cirrose. As doenças hepáticas crônicas são uma questão de saúde global crucial e a causa de aproximadamente 2 milhões de mortes por ano em todo o mundo. A cirrose, hoje em dia, é a 11ª causa mais comum de morte globalmente. O tratamento da célula-tronco mesenquimal (MSCs) é uma maneira eletiva de tratar a doença hepática aguda e crônica. O objetivo deste estudo é melhorar o potencial terapêutico dos MSCs combinados com a melatonina (MLT) para superar a fibrose hepática induzida por CCl4 e também investigar o impacto individual da melatonina e MSCs contra o comprometimento do fígado induzido por CCl4 no modelo animal. Os ratos BALB / C fêmeas foram usados ​​como modelo de animal fibrótico de fígado induzido por CCl4. Cinco grupos de modelo animal foram feitos: Controle Negativo, Controle Positivo, CCl4 + MSCs Tratados Grupo, Grupo Tratado CCl4 + MLT e Grupo Tratado CCl4 + MSCs + MLT. MSCs cultivados da medula óssea dos ratos foram transplantados para o modelo de camundongos de fígado induzido por CCl4, individualmente, bem como em conjunto com a melatonina. Duas semanas após a administração MSCs e MLT, todos os grupos de camundongos foram sacrificados para o exame. Os resultados morfológicos e histopatológicos mostraram que a terapia combinada do MSCs + MLT mostrou impacto benéfico substancial no modelo ferido no fígado induzido pelo CCl4, em comparação com o MSCs e o MLT individualmente. A redução bioquimicamente considerável foi observada em bilirrubina sérica e níveis ALT de ratinhos tratados com MLT + MSCs, em comparação com outros grupos. Os resultados de PCR mostraram regulação negativa do BAX e regulação positiva do BCL-XL e da albumina, confirmando um efeito terapêutico significativo do MSCs + MLT na fibrose hepática induzida por CCl4. Dos resultados, conclui-se que a terapia combinada de MSCs e MLT mostram um forte efeito terapêutico na fibrose hepática induzida por CCl4, em comparação com MSCs e MLT individualmente.

Producción científica en investigación sobre avances terapéuticos de la Enfermedad de Peyronie durante los últimos 62 años. Un análisis bibliométrico / Scientific production on research on therapeutic advances in Peyronie's Disease during the last 62 Years. A bibliometric analysis / Produção científica em pesquisa sobre avanços terapêuticos na Doença de Peyronie nos últimos 62 anos. Uma análise bibliométrica

Introducción. La enfermedad de Peyronie es una malformación adquirida del pene, originada por la deposición de placas fibróticas en la túnica albugínea. La prevalencia en Estados Unidos oscila entre el 0.39% y 11.8%, en Europa 8.9%, en Latinoamérica no existe un porcentaje puntual de prevalencia actual debido a la escasez de reportes de esta patología. Este análisis bibliométrico busca describir la evolución terapéutica de la Enfermedad de Peyronie en la literatura de los últimos 62 años, así como la distribución geográfica de estas publicaciones. Metodología. Estudio observacional, descriptivo, un análisis bibliométrico desde 1957 hasta 2019, utilizando GoPubMed y FABUMED. Resultados. Se obtuvieron 721 referencias sobre tratamiento quirúrgico en enfermedad de Peyronie, con un aumento de la producción científica a lo largo del periodo de estudio. The Journal of Urology fue la revista con mayor cantidad de publicaciones, el 57.9% dentro de la categoría de artículo científico. El país líder fue Estados Unidos con 191 publicaciones. Discusión. Existe poca literatura sobre los avances terapéuticos para el tratamiento de enfermedad de Peyronie, lo que dificulta la comparación de las investigaciones a lo largo de los años en diferentes zonas del mundo. La investigación en Latinoamérica es escasa. Conclusión. La investigación sobre el tratamiento quirúrgico en enfermedad de Peyronie muestra un patrón ascendente en la productividad científica durante los años estudiados. Los países con mayores ingresos económicos son de mayor desarrollo en el tema y en menor medida regiones con recursos limitados. El análisis evidencia la importancia de aumentar producción científica en Colombia, así como estimular la investigación sobre este tema, ya que existen muy pocas publicaciones sobre la evolución del tratamiento quirúrgico para esta enfermedad. Palabras clave: Induración Peniana; Enfermedades del Pene; Bibliometría; Fibrosis; Erección Peniana

Introduction. Peyronie's disease is an acquired malformation of the penis, caused by the deposition of fibrotic plaques in the tunica albuginea. The prevalence in the United States ranges between 0.39% and 11.8%, in Europe 8.9%, in Latin America there is no specific percentage of current prevalence due to the scarcity of reports of this pathology. This bibliometric analysis seeks to describe the therapeutic evolution of Peyronie's Disease in the literature over the last 62 years, as well as the geographic distribution of these publications. Methodology. This is an observational, descriptive study, with a bibliometric analysis from 1957 to 2019, using GoPubMed and FABUMED. Results. 721 references on surgical treatment in Peyronie's disease were obtained, with an increase in scientific production throughout the study period. The Journal of Urology was the journal with the highest number of publications, 57.9% within the scientific article category. The leading country was the United States with 191 publications. Discussion. There is a limited amount of literature on therapeutic advances for the treatment of Peyronie's disease, which makes it difficult to compare research over the years in different areas of the world. Research in Latin America is scarce. Conclusion. Research on surgical treatment in Peyronie's disease shows an increasing pattern in scientific productivity over the years. Countries with higher economic income have greater development in the subject and to a lesser extent regions with limited resources. The analysis shows the importance of increasing scientific production in Colombia, as well as stimulating research on this topic, since there are few publications on the evolution of surgical treatment for this disease. Keywords: Penile Induration; Penile Diseases; Bibliometrics; Fibrosis; Penile Erection

Introdução. A doença de Peyronie é uma malformação adquirida do pênis, causada pela deposição de placas fibróticas na túnica albugínea. A prevalência nos Estados Unidos varia entre 0.39% e 11.8%, na Europa 8.9%, na América Latina não existe um percentual específico de prevalência atual devido à escassez de relatos desta patologia. Esta análise bibliométrica tem como objetivo descrever a evolução terapêutica da Doença de Peyronie na literatura dos últimos 62 anos, bem como a distribuição geográfica destas publicações. Metodologia. Estudo observacional, descritivo, análise bibliométrica de 1957 a 2019, utilizando GoPubMed e FABUMED. Resultados. Foram obtidas 721 referências sobre tratamento cirúrgico na doença de Peyronie, com aumento da produção científica ao longo do período do estudo. The Journal of Urology foi o periódico com maior número de publicações, 57.9% dentro da categoria artigo científico. O país líder foram os Estados Unidos com 191 publicações. Discussão. Há pouca literatura sobre avanços terapêuticos para o tratamento da doença de Peyronie, o que dificulta a comparação de pesquisas ao longo dos anos em diferentes partes do mundo. As pesquisas na América Latina são escassas. Conclusão. As pesquisas sobre o tratamento cirúrgico da doença de Peyronie mostram um padrão crescente de produtividade científica ao longo dos anos estudados. Os países com maior rendimento económico são mais desenvolvidos no assunto e, em menor medida, regiões com recursos limitados. A análise mostra a importância de aumentar a produção científica na Colômbia, bem como estimular a pesquisa sobre o tema, uma vez que existem poucas publicações sobre a evolução do tratamento cirúrgico desta doença. Palavras-chave: Induração Peniana; Doenças do Pênis; Bibliometria; Fibrose; Ereção Peniana

Captopril inhibits thioacetamide-induced chronic liver injury associated with the suppression of inflammation / hypoxia- inducible factor 1-alpha / profibrogenic axis-mediated hepatotoxicity in rats / Captopril inhibe la lesión hepática crónica inducida por tioacetamida asociada con la supresión de la inflamación/factor 1-alfa inducible por hipoxia/hepatotoxicidad mediada por el eje profibrogénico en rata

SUMMARY: Liver transplantation is the only available method to treat liver failure induced by chronic liver injury. We sought to determine whether the angiotensin-converting enzyme inhibitor, captopril, can inhibit the development of chronic liver injury induced by the hepatotoxic agent thioacetamide (TAA) in association with the suppression of inflammation (hsCRP, TNF-α, and IL-6) / hypoxia- inducible factor 1-alpha (HIF-1α) / profibrosis (TIMP-1, MMP-9, and α-SMA) axis that mediates liver injury. Therefore, the model group of rats was injected for eight weeks with 200 mg/kg TAA starting at week two. The protective group was pretreated with 150 mg/ kg captopril daily for two weeks prior to TAA injections and continued receiving both capropril and TAA agents until being humanely scrificed at week 10. We observed a substantial damage to liver tissue in the model group as demonstrated by a significant (p<0.0001) increase in blood and hepatic tissue levels of high sensitivity C-reactive protein (hsCRP), tumor necrosis factor-a (TNF-α), interleukin- 6 (L-6), HIF-1α, tissue inhibitor of metalloproteinases-1 (TIMP-1), matrix metalloproteinase-9 (MMP-9), alpha-smooth muscle actin (α-SMA), alanine aminotransferase (ALT), and aspartate aminotransferase (AST). All these parameters were significantly (p<0.0244) protected by captopril. Also, a significant (p<0.0001) positive correlation was observed between a-SMA (profibrosis) and the serum and tissue levels of hsCRP, TNF-α, HIF-1α, TIMP-1, MMP-9, and ALT. Thus, these findings suggest that the induction of chronic liver injury by the hepatotoxic compound, TAA is associated with the upregulation of inflammation/HIF-1α/profibrosis, with captopril exhibiting beneficial hepatic pleotropic effects.

El trasplante de hígado es el único método disponible para tratar la insuficiencia hepática inducida por una lesión hepática crónica. Buscamos determinar si el inhibidor de la enzima convertidora de angiotensina, captopril, puede inhibir el desarrollo de lesión hepática crónica inducida por el agente hepatotóxico tioacetamida (TAA) en asociación con la supresión de la inflamación (hsCRP, TNF-α e IL-6) / factor inducible por hipoxia 1-alfa (HIF-1α) / profibrosis (TIMP-1, MMP-9 y α- SMA) eje que media la lesión hepática. Por lo tanto, al grupo modelo de ratas se le inyectó durante ocho semanas 200 mg/kg de TAA a partir de la semana dos. El grupo protector fue pretratado con 150 mg/kg de captopril al día durante dos semanas antes de las inyecciones de TAA y continuó recibiendo capropril y agentes TAA hasta que fue sacrificado en la semana 10. Observamos un daño sustancial en el tejido hepático en el grupo modelo, como lo demuestra un aumento significativo (p<0,0001) de los niveles en sangre y tejido hepático de proteína C reactiva de alta sensibilidad (hsCRP), factor de necrosis tumoral-α (TNF-a), interleucina-6 (L-6), HIF-1α, inhibidor tisular de metaloproteinasas-1 (TIMP-1), metaloproteinasa de matriz-9 (MMP-9), actina de músculo liso alfa (α-SMA), alanina aminotransferasa (ALT) y aspartato aminotransferasa (AST). Todos estos parámetros estaban significativamente (p<0,0244) protegidos por captopril. Además, se observó una correlación positiva significativa (p<0,0001) entre α-SMA (profibrosis) y los niveles séricos y tisulares de hsCRP, TNF-α, HIF-1α, TIMP- 1, MMP-9 y ALT. Por lo tanto, estos hallazgos sugieren que la inducción de daño hepático crónico por el compuesto hepatotóxico, TAA, está asociada con la regulación al alza de la inflamación/HIF-1α/profibrosis, con captopril exhibiendo efectos pleotrópicos hepáticos beneficiosos.

A rat model of rheumatoid arthritis: TDZD-8 is associated with the protection against the induction of the synovium knee joint IL-17A/GSK3beta/ROS/alpha-SMA axis of fibrosis / Un modelo de rata de artritis reumatoide: TDZD-8 está asociado con la protección contra la inducción del eje de fibrosis de la articulación sinovial de la rodilla IL-17A/GSK3ß/ROS/α-SMA

SUMMARY: Rheumatoid arthritis (RA) that affects the synovial knee joint causes swelling of the synovial membrane and tissue damage. Interleukin-17A (IL-17A) and the enzyme glycogen synthase kinase-3β (GSK3β) are involved in the pathogenesis of RA. The link between IL-17A, GSK3β, the oxidative stress, and the profibrogenic marker alpha-smooth muscle actin (α-SMA) with and without TDZD-8, GSK3β inhibitor has not been studied before. Consequently, active immunization of rats was performed to induce RA after three weeks using collagen type II (COII) injections. The treated group received daily injection of 1 mg/kg TDZD-8 for 21 days following the immunization protocol (COII+TDZD-8). Blood and synovium tissue samples were harvested at the end of the experiment. RA development was confirmed as corroborated by a substantial increase in blood levels of the highly specific autoantibody for RA, anti-citrullinated protein antibody as well as augmentation of reactive oxidative species (ROS) levels measured as lipid peroxidation. RA induction also increased synovium tissue levels of IL-17A and the profibrogenic marker, α-SMA. All these parameters seemed to be significantly (p<0.0001) ameliorated by TDZD-8. Additionally, a significant correlation between IL-17A, ROS, and α-SMA and biomarkers of RA was observed. Thus, knee joint synovium RA induction augmented IL-17A/GSK3β/ROS/α-SMA axis mediated arthritis in a rat model of RA, which was inhibited by TDZD-8.

La artritis reumatoide (AR) que afecta la articulación sinovial de la rodilla provoca inflamación de la membrana sinovial y daño tisular. La interleucina-17A (IL-17A) y la enzima glucógeno sintasa quinasa-3β (GSK3β) están involucradas en la patogenia de la AR. No se ha estudiadol vínculo entre IL-17A, GSK3β, el estrés oxidativo y el marcador profibrogénico actina de músculo liso alfa (α-SMA) con y sin inhibidor de TDZD-8, GSK3β. En consecuencia, se realizó una inmunización activa de ratas para inducir la AR después de tres semanas usando inyecciones de colágeno tipo II (COII). El grupo tratado recibió una inyección diaria de 1 µg/ kg de TDZD-8 durante 21 días siguiendo el protocolo de inmunización (COII+TDZD-8). Se recogieron muestras de sangre y tejido sinovial al final del experimento. El desarrollo de AR se confirmó como lo corroboró el aumento sustancial en los niveles sanguíneos del autoanticuerpo altamente específico para AR, el anticuerpo antiproteína citrulinada, así como el aumento de los niveles de especies oxidativas reactivas (ROS) medidos como peroxidación lipídica. La inducción de AR también aumentó los niveles de tejido sinovial de IL-17A y el marcador profibrogénico, α-SMA. Todos estos parámetros parecían mejorar significativamente (p<0,0001) con TDZD-8. Además, se observó una correlación significativa entre IL- 17A, ROS y α-SMA y biomarcadores de AR. Por lo tanto, la inducción de AR en la sinovial de la articulación de la rodilla aumentó la artritis mediada por el eje IL-17A/GSK3β/ROS/α-SMA en un modelo de rata de AR, que fue inhibida por TDZD-8.

Rinofima: reporte de un caso de Clínica Estrella / Rhinophyma: a case report of Clínica Estrella

La rinofima es una patología que se caracteriza por presentar hipertrofia de las glándulas sebáceas con proliferación de tejido fibroso, donde la nariz toma un aspecto lobulado dando como resultado la deformidad de la punta nasal; es una forma de rosácea. La prevalencia de esta variedad de rosácea es de aproximadamente un 5-7% en la población y con predominio en el sexo masculino de la quinta a séptima década de vida. Su etiología no se conoce con exactitud. Se presenta el caso de un paciente masculino de 84 años, con antecedentes patológicos de hipertensión arterial e hipotiroidismo; su lesión inició hace 10 años, como una lesión eritematosa con presencia de telangiectasia a nivel de alas y punta nasal, no dolorosa. Se realizó tratamiento con bisturí frío y radiofrecuencia, se realizaron cortes transversales hasta dejar el lecho desprovisto del tumor y finalmente se usó radiofrecuencia en toda la superficie de la lesión restante. Se realizó el procedimiento ambulatorio sin complicaciones inmediatas o tardías

Rhinophyma is a pathology characterized by hypertrophy of the sebaceous glands with proliferation of fibrous tissue, the nose has a lobed appearance, as a result there is a deformity of the nasal tip; rhinophyma is a form of rosacea. The prevalence of this variety of rosacea is approximately 5-7% in the population and predominantly in males from the fifth to seventh decade of life, the etiology is not well known, however there are several predisposing genetic and environmental factors. We present the case of an 84-year-old male patient with a pathological history of arterial hypertension and hypothyroidism; his lesion began 10 years ago, as an erythematous lesion with presence of telangiectasia in the wings and nasal tip, not painful. Treatment was performed with a cold scalpel and radiofrequency, transverse cuts were made until the tumor was gone, and finally radiofrequency was used on the entire surface of the remaining lesion. The outpatient procedure was performed without immediate or late complications.

Inflammatory Fibrous Hyperplasia Associated with Chondroid Metaplasia - Report and Morphological Analysis of Five Cases / Hiperplasia Fibrosa Inflamatoria Asociada a Metaplasia Cartilaginosa - Reporte y Análisis Morfológico de Cinco Casos

Inflammatory fibrous hyperplasia (IFH) is a common reactive lesion in dental prostheses users that may be associated with chondroid metaplasia (CM). Metaplasia is an adaptive cellular process that may be caused by trauma. We reported here five cases of IFH associated with CM and analyzed morphologically the deposition of collagen in these lesions. Patients had a mean age of 58.8 years-old and were ill-fitting dental prostheses users. They presented nodular lesions located in the anterior maxilla. Microscopically, it was observed hyperplastic fibrous connective tissue with chronic inflammatory infiltrate and hyaline cartilage. No morphological differences were observed in collagen deposition under light microscopy, but quantitative analysis revealed a significantly higher collagen deposition at the connective tissue near CM (p = 0.015). IFH associated with CM affects ill-fitting dental prostheses users. The presence of CM is not significant to the lesion prognosis. However, its formation and the higher collagen deposition near it reinforces the IFH reactive origin.

La hiperplasia fibrosa inflamatoria (HFI) es una lesión reactiva común en los usuarios de prótesis dentales que puede estar asociada con la metaplasia cartilaginosa (MC). La metaplasia es un proceso celular adaptativo que puede ser causado por un trauma. El presente informe analizó cinco casos de HFI asociados a MC y se analizaron morfológicamente la deposición de colágeno en estas lesiones. Los pacientes tenían una edad media de 58,8 años y eran usuarios de prótesis dentales mal adaptadas. Se observaron lesiones nodulares localizadas en el la parte anterior del maxilar Microscópicamente se observó tejido conectivo fibroso hiperplásico con infiltrado inflamatorio crónico y cartílago hialino. No se observaron diferencias morfológicas en la deposición de colágeno bajo microscopía óptica, pero el análisis cuantitativo reveló una deposición de colágeno significativamente mayor en el tejido conectivo cerca de MC (p = 0,015). La HFI asociada con la MC afecta a los usuarios de prótesis dentales mal adaptadas. La presencia de MC no es significativa para el pronóstico de la lesión. Sin embargo, su formación y la mayor deposición de colágeno cerca de MC refuerza el origen reactivo de HFI.

Variaciones morfológicas de la glándula submandibular en ratas obesas por acción de glutamato monosódico / Morphological variations of the submandibular gland in obese rats by the action of monosodium glutamate

Este estudio tuvo como objetivo demostrar la existencia de variaciones morfológicas en el tejido conectivo de la glándula submandibular de ratas obesas expuestas a glutamato monosódico (GMS). Se utilizaron 12 ratas Sprague Dawley machos recién nacidas (6 ratas para el grupo 1, control; 6 ratas para el grupo 2 (GMS), 4 mg/g de glutamato monosódico de peso (5 dosis) mantenidas por 16 semanas respectivamente con una dieta y agua ad libitum. En el estudio se realizó un análisis estereológico e histológico, demostrándose una variación en el tejido conectivo presentando una disminución del volúmen glandular, mayor fibrosis, y disminución de adipocitos a nivel periférico siendo reemplazado por tejido rico en colágeno. Los vasos sanguíneos observados a nivel estereológico no presentan mayores cambios en cuanto a volumen, superficie y área.

SUMMARY: This study aims to demonstrate the existence of morphological variations in the connective tissue of the submandibular gland of obese rats exposed to MSG. Twelve male newborn Sprague Dawley rats were used (6 rats for group 1, control; 6 rats for group 2 (MSG), 4 mg/g of monosodium glutamate of weight (5 doses) maintained for 16 weeks respectively with a diet and water ad libitum. In the study, a stereological and histological analysis was carried out, demonstrating a variation in the connective tissue, presenting a decrease in the glandular volume, greater fibrosis, and a decrease in adipocytes at the peripheral level, being replaced by tissue rich in collagen. Blood cells observed at the stereological level do not present major changes in terms of volume, surface and area, but in the histological study greater vascularization is observed.

Inhibition of glutaminolysis alleviates myocardial fibrosis induced by angiotensin II / 生理学报

The present study was aimed to investigate the role and mechanism of glutaminolysis of cardiac fibroblasts (CFs) in hypertension-induced myocardial fibrosis. C57BL/6J mice were administered with a chronic infusion of angiotensin II (Ang II, 1.6 mg/kg per d) with a micro-osmotic pump to induce myocardial fibrosis. Masson staining was used to evaluate myocardial fibrosis. The mice were intraperitoneally injected with BPTES (12.5 mg/kg), a glutaminase 1 (GLS1)-specific inhibitor, to inhibit glutaminolysis simultaneously. Immunohistochemistry and Western blot were used to detect protein expression levels of GLS1, Collagen I and Collagen III in cardiac tissue. Neonatal Sprague-Dawley (SD) rat CFs were treated with 4 mmol/L glutamine (Gln) or BPTES (5 μmol/L) with or without Ang II (0.4 μmol/L) stimulation. The CFs were also treated with 2 mmol/L α-ketoglutarate (α-KG) under the stimulation of Ang II and BPTES. Wound healing test and CCK-8 were used to detect CFs migration and proliferation respectively. RT-qPCR and Western blot were used to detect mRNA and protein expression levels of GLS1, Collagen I and Collagen III. The results showed that blood pressure, heart weight and myocardial fibrosis were increased in Ang II-treated mice, and GLS1 expression in cardiac tissue was also significantly up-regulated. Gln significantly promoted the proliferation, migration, mRNA and protein expression of GLS1, Collagen I and Collagen III in the CFs with or without Ang II stimulation, whereas BPTES significantly decreased the above indices in the CFs. α-KG supplementation reversed the inhibitory effect of BPTES on the CFs under Ang II stimulation. Furthermore, in vivo intraperitoneal injection of BPTES alleviated cardiac fibrosis of Ang II-treated mice. In conclusion, glutaminolysis plays an important role in the process of cardiac fibrosis induced by Ang II. Targeted inhibition of glutaminolysis may be a new strategy for the treatment of myocardial fibrosis.

Shenmai Injection Improves Hypertensive Heart Failure by Inhibiting Myocardial Fibrosis via TGF-β 1/Smad Pathway Regulation / 中国结合医学杂志

OBJECTIVE@#To study effects of Shenmai Injection on hypertensive heart failure and its mechanism for inhibiting myocardial fibrosis.@*METHODS@#Salt-sensitive (Dahl/SS) rats were fed with normal diet (0.3% NaCl) and the high-salt diet (8% NaCl) to observe the changes in blood pressure and heart function, as the control group and the model group. Salt-insensitive rats (SS-13BN) were fed with the high-salt diet (8% NaCl) as the negative control group. After modeling, the model rats were randomly divided into heart failure (HF) group, Shenmai Injection (SMI) group and pirfenidone (PFD) group by a random number table, with 6 rats in each group. They were given sterilized water, SMI and pirfenidone, respectively. Blood pressure, cardiac function, fibrosis and related molecular expression were detected by sphygmomanometer, echocardiogram, enzyme linked immunosorbent assay (ELISA), hematoxylin-eosin staining, Masson staining, immunofluorescence and qPCR analysis.@*RESULTS@#After high-salt feeding, compared with the control and negative control group, in the model group the blood pressure increased significantly, the left ventricular ejection fraction (LVEF) and left ventricular fraction shortening (LVFS) were significantly reduced, and the serum NT-proBNP concentration increased significantly (all P<0.05); furthermore, the arrangement of myocardial cells was disordered, the edema was severe, and the degree of myocardial fibrosis was also significantly increased (P<0.05); the protein and mRNA expressions of collagen type I (Col I) were up-regulated (P<0.05), and the mRNA expressions of transforming growth factor β 1 (TGF- β 1), Smad2 and Smad3 were significantly up-regulated (P<0.05). Compared with HF group, after intervention of Shenmai Injection, LVEF and LVFS increased, myocardial morphology was improved, collagen volume fraction decreased significantly (P<0.05), and the mRNA expressions of Col I, TGF- β 1, Smad2 and Smad3, as well as Col I protein expression, were all significantly down-regulated (all P<0.05).@*CONCLUSION@#Myocardial fibrosis is the main pathological manifestation of hypertensive heart failure, and Shenmai Injection could inhibit myocardial fibrosis and effectively improve heart failure by regulating TGF-β 1/Smad signaling pathway.

Involvement of Interleukin-1 β/Insulin-Like Growth Factor 1 in Ameliorating Effects of Electroacupuncture on Myocardial Fibrosis Induced by Essential Hypertension / 中国结合医学杂志

OBJECTIVE@#To investigate the effect of electroacupuncture (EA) at Neiguan (PC 6) on myocardial fibrosis in spontaneously hypertensive rats (SHRs), and to explore the contribution of interleukin-1 β (IL-1 β), insulin-like growth factor 1 (IGF-1), and transforming growth factor β 1 (TGF- β 1) to the effects.@*METHODS@#Nine 12-weeks-old Wistar Kyoto (WKY) male rats were employed as the normal group. Twenty-seven SHRs were equally randomized into SHR, SHR+EA, and SHR + sham groups. EA was applied at bilateral PC 6 once a day 30 min per day in 8 consecutive weeks. After 8-weeks EA treatment at PC 6, histopathologic changes of collagen type I (Col I), collagen type 1 (Col 1) and the levels of IGF-1, 1L-1 β, TGF- β 1, matrix metalloproteinase (MMP)-2 and MMP-9 were examined in myocardial tissure respectively.@*RESULTS@#After 8-weeks EA treatment at PC 6, the enhanced myocardial fibrosis in SHRs were characterized by the increased mean fluorescence intensity of Col I and Col 1 in myocardium tissue (P<0.01). All these abnormal alterations above in SHR + EA group was significantly lower compared with the SHR group (P<0.01). Meanwhile, the increased levels of IL-1 β, IGF-1, TGF-β 1 in serum or myocardial tissue of SHRs, diminished MMP 9 mRNA expression in SHRs were also markedly inhibited after 8 weeks of EA treatment (P<0.05 or P<0.01). Furthermore, the contents of IL-1 β, IGF-1, TGF-β 1 in myocardial tissue were positively correlated with the systolic blood pressure and hydroxyproline respectively (P<0.01).@*CONCLUSION@#EA at bilateral PC 6 could ameliorate cardiac fibrosis in SHRs, which might be mediated by regulation of 1L-1 β/IGF-1-TGF- β 1-MMP9 pathway.

Spatiotemporal Dynamics of the Molecular Expression Pattern and Intercellular Interactions in the Glial Scar Response to Spinal Cord Injury / 神经科学通报·英文版

Nerve regeneration in adult mammalian spinal cord is poor because of the lack of intrinsic regeneration of neurons and extrinsic factors - the glial scar is triggered by injury and inhibits or promotes regeneration. Recent technological advances in spatial transcriptomics (ST) provide a unique opportunity to decipher most genes systematically throughout scar formation, which remains poorly understood. Here, we first constructed the tissue-wide gene expression patterns of mouse spinal cords over the course of scar formation using ST after spinal cord injury from 32 samples. Locally, we profiled gene expression gradients from the leading edge to the core of the scar areas to further understand the scar microenvironment, such as neurotransmitter disorders, activation of the pro-inflammatory response, neurotoxic saturated lipids, angiogenesis, obstructed axon extension, and extracellular structure re-organization. In addition, we described 21 cell transcriptional states during scar formation and delineated the origins, functional diversity, and possible trajectories of subpopulations of fibroblasts, glia, and immune cells. Specifically, we found some regulators in special cell types, such as Thbs1 and Col1a2 in macrophages, CD36 and Postn in fibroblasts, Plxnb2 and Nxpe3 in microglia, Clu in astrocytes, and CD74 in oligodendrocytes. Furthermore, salvianolic acid B, a blood-brain barrier permeation and CD36 inhibitor, was administered after surgery and found to remedy fibrosis. Subsequently, we described the extent of the scar boundary and profiled the bidirectional ligand-receptor interactions at the neighboring cluster boundary, contributing to maintain scar architecture during gliosis and fibrosis, and found that GPR37L1_PSAP, and GPR37_PSAP were the most significant gene-pairs among microglia, fibroblasts, and astrocytes. Last, we quantified the fraction of scar-resident cells and proposed four possible phases of scar formation: macrophage infiltration, proliferation and differentiation of scar-resident cells, scar emergence, and scar stationary. Together, these profiles delineated the spatial heterogeneity of the scar, confirmed the previous concepts about scar architecture, provided some new clues for scar formation, and served as a valuable resource for the treatment of central nervous system injury.

Meta-analysis of Ac-SDKP inhibition of Pulmonary fibrosis in animal models / 中华劳动卫生职业病杂志

Objective: To systematically study the anti-fibrotic effect of N-acetyl-seryl-as partyl-lysyl-proline (Ac-SDKP) on pulmonary fibrosis. Methods: In May 2021, a computer search was performed on CNKI, Wanfang Knowledge Service Platform, VIP.com, China Biomedical Literature Database, Pubmed, OVID and other databases. The retrieval time was from January 2008 to May 2021. Randomized controlled experiments on the inhibition of pulmonary fibrosis by Ac-SDKP were screened. The control group was the pulmonary fibrosis model group and the experimental group was the Ac-SDKP treatment group. The quality of the literature was assessed using the syrcle risk of bias assessment tool, and data were extracted. Data analysis was Performed using revman 5.4 software. Results: 18 papers were included, with a total of 428 animal models. The results of meta analysis showed that the contents of α-smooth muscle actin (α-SMA), type I collagen, type Ⅲ collagen, transforming growth factor-β (TGF-β) and Nodule area in the exPerimental group were lower than those in the control grouP. [SMD=-2.44, 95%CI (-3.71--1.17), P=0.000][SMD=-5.36, 95%CI (-7.13--3.59), P=0.000] [SMD=-3.07, 95%CI (-4.13--2.02), P<0.000][SMD=-2.88, 95%CI (-3.63--2.14), P=0.000] [SMD=-1.80, 95%CI (-2.42--1.18), P=0.000], the content of hydroxy proline in the experimental group was higher than that in the control group [SMD=7.62, 95%CI (4.90-10.33), P=0.000], all indexes included in the literature were statistically significant. Conclusion: Ac-SDKP has obvious inhibitory effect on the process of pulmonary fibrosis, and may become a new clinical drug for the treatment of pulmonary fibrosis.

Research progress on the histological scoring system for nonalcoholic fatty liver disease / 中华肝脏病杂志

Non-alcoholic fatty liver disease (NAFLD) has replaced chronic hepatitis B as the most common chronic liver disease in China and has now been renamed metabolic dysfunction-associated fatty liver disease (MAFLD). The Brunt, the American NASH Clinical Research Network (NASH-CRN), the European Steatosis, Activity, and Fibrosis/Fatty Liver Inhibition of Progression (SAF/FLIP), and the Pediatric NAFLD are currently the four semi-quantitative grading systems for histological evaluation. This paper reviews these four scoring systems for the clinical selection of appropriate systems for diagnosis and prognosis assessment. This article is a review, and in order to coordinate the evaluation criteria of various scoring systems, the old name "NAFLD" is used.