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The endoplasmic reticulum, a key cellular organelle, regulates a wide variety of cellular activities. Endoplasmic reticulum autophagy, one of the quality control systems of the endoplasmic reticulum, plays a pivotal role in maintaining endoplasmic reticulum homeostasis by controlling endoplasmic reticulum turnover, remodeling, and proteostasis. In this review, we briefly describe the endoplasmic reticulum quality control system, and subsequently focus on the role of endoplasmic reticulum autophagy, emphasizing the spatial and temporal mechanisms underlying the regulation of endoplasmic reticulum autophagy according to cellular requirements. We also summarize the evidence relating to how defective or abnormal endoplasmic reticulum autophagy contributes to the pathogenesis of neurodegenerative diseases. In summary, this review highlights the mechanisms associated with the regulation of endoplasmic reticulum autophagy and how they influence the pathophysiology of degenerative nerve disorders. This review would help researchers to understand the roles and regulatory mechanisms of endoplasmic reticulum-phagy in neurodegenerative disorders.
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Neurons rely heavily on high mitochondrial metabolism to provide sufficient energy for proper development. However, it remains unclear how neurons maintain high oxidative phosphorylation (OXPHOS) during development. Mitophagy plays a pivotal role in maintaining mitochondrial quality and quantity. We herein describe that G protein-coupled receptor 50 (GPR50) is a novel mitophagy receptor, which harbors the LC3-interacting region (LIR) and is required in mitophagy under stress conditions. Although it does not localize in mitochondria under normal culturing conditions, GPR50 is recruited to the depolarized mitochondrial membrane upon mitophagy stress, which marks the mitochondrial portion and recruits the assembling autophagosomes, eventually facilitating the mitochondrial fragments to be engulfed by the autophagosomes. Mutations Δ502-505 and T532A attenuate GPR50-mediated mitophagy by disrupting the binding of GPR50 to LC3 and the mitochondrial recruitment of GPR50. Deficiency of GPR50 causes the accumulation of damaged mitochondria and disrupts OXPHOS, resulting in insufficient ATP production and excessive ROS generation, eventually impairing neuronal development. GPR50-deficient mice exhibit impaired social recognition, which is rescued by prenatal treatment with mitoQ, a mitochondrially antioxidant. The present study identifies GPR50 as a novel mitophagy receptor that is required to maintain mitochondrial OXPHOS in developing neurons.
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Mitocôndrias , Mitofagia , Neurônios , Receptores Acoplados a Proteínas G , Animais , Receptores Acoplados a Proteínas G/metabolismo , Receptores Acoplados a Proteínas G/genética , Neurônios/metabolismo , Mitocôndrias/metabolismo , Camundongos , Humanos , Fosforilação Oxidativa , Proteínas Associadas aos Microtúbulos/metabolismo , Proteínas Associadas aos Microtúbulos/genética , Espécies Reativas de Oxigênio/metabolismo , Camundongos Knockout , NeurogêneseRESUMO
Colorectal cancer (CRC) is the third most common cancer worldwide and the second most common cause of cancer death. Nanotherapies are able to selectively target the delivery of cancer therapeutics, thus improving overall antitumor efficiency and reducing conventional chemotherapy side effects. Mesoporous silica nanoparticles (MSNs) have attracted the attention of many researchers due to their remarkable advantages and biosafety. We offer insights into the recent advances of MSNs in CRC treatment and their potential clinical application value.
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Objective: To explore the association between the variant mutations within embB and ubiA, and the degree of ethambutol (EMB) resistance of Mycobacterium tuberculosis (M. tuberculosis) isolates. Methods: A total of 146 M. tuberculosis isolates were used to determine the minimum inhibitory concentrations (MICs) of EMB with a 96-well microplate-based assay. The mutations within embB and ubiA among these isolates were identified with DNA sequencing. Moreover, a multivariate regression model and a computer model were established to assess the effects of mutations on EMB resistance. Results: Our data showed that overall 100 isolates exhibited 28 mutated patterns within the sequenced embB and ubiA. Statistical analysis indicated that embB mutations Met306Val, Met306Ile, Gly406Ala, and Gln497Arg, were strongly associated with EMB resistance. Of these mutations, Met306Val and Gln497Arg were significantly associated with high-level EMB resistance. Almost all multiple mutations occurred in high-level EMB-resistant isolates. Although the mutation within ubiA accompanied with embB mutation presented exclusively in EMB-resistant isolates, four single ubiA mutations (Ala39Glu, Ser173Ala, Trp175Cys, and Val283Leu) leading to protein instability were observed in EMB-susceptible isolates. Conclusion: This study highlighted the complexity of EMB resistance. Some individual mutations and multiple mutations within embB and ubiA contributed to the different levels of EMB resistance.
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BACKGROUND: Patients with Turner syndrome (TS) face an increased risk of developing aortic dilatation (AD), but diagnosing AD in children presents greater complexity compared to adults. This study aimed to investigate the application of various assessment indicators of AD in Chinese children and adolescents with TS. METHODS: This study included TS patients admitted to Shenzhen Children's Hospital from 2017 to 2022. Cardiovascular lesions were diagnosed by experienced radiologists. Patients without structural heart disease were divided into different body surface area groups, then the Chinese TS population Z-score (CHTSZ-score) of the ascending aorta was calculated and compared with other indicators such as aortic size index (ASI), ratio of the ascending to descending aortic diameter (A/D ratio), and TSZ-score (Quezada's method). RESULTS: A total of 115 TS patients were included, with an average age of 10.0 ± 3.7 years. The incidences of the three most serious cardiovascular complications were 9.6% (AD), 10.4% (coarctation of the aorta, CoA), and 7.0% (bicuspid aortic valve, BAV), respectively. The proportion of developing AD in TS patients aged ≥ 10 years was higher than that in those < 10 years old (16.6% vs. 1.8%, P = 0.009), and the proportion of patients with CoA or BAV who additionally exhibited AD was higher than those without these conditions (31.6% vs. 5.2%, P < 0.001). The ASI, A/D ratio, TSZ-score, and CHTSZ-score of the 11 patients with AD were 2.27 ± 0.40 cm/m2, 1.90 ± 0.37, 1.28 ± 1.08, and 3.07 ± 2.20, respectively. Among the AD patients, only 3 cases had a TSZ-score ≥ 2, and 2 cases had a TSZ-score ≥ 1. However, based on the assessment using the CHTSZ-score, 6 patients scored ≥ 2, and 5 patients scored ≥ 1. In contrast, the TSZ-score generally underestimated the aortic Z-scores in Chinese children with TS compared to the CHTSZ-score. CONCLUSIONS: The applicability of ASI and A/D ratio to children with TS is questionable, and racial differences can affect the assessment of TSZ-score in the Chinese population. Therefore, establishing the CHTSZ-score specifically tailored for Chinese children and adolescents is of paramount importance.
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Síndrome de Turner , Humanos , Síndrome de Turner/complicações , Criança , Adolescente , Feminino , China/epidemiologia , Dilatação Patológica/etiologia , Masculino , Estudos Retrospectivos , Aorta/patologia , Aorta/diagnóstico por imagem , Coartação Aórtica , Doença da Válvula Aórtica Bicúspide/complicações , Pré-Escolar , Incidência , População do Leste AsiáticoRESUMO
CONTEXT: Childhood and adolescence are critical periods for lifelong bone health. The impact of obesity on these phases is controversial, which may be due to the lack of standards for age-, sex-, and puberty-specific Bone turnover markers (BTMs) which could sensitively reflect bone metabolism. OBJECTIVE: To generate age-, sex, and puberty stage-specific BTMs reference curves in children and adolescents and to explore the effect of obesity on bone metabolism in the Chinese population. METHODS: Our study was part of the Evaluation and Monitoring on School-based Nutrition and Growth in Shenzhen study. 800 participants aged 6â¼18 years with normal body mass index (BMI) were selected to establish BTM reference curves for boys and girls at different ages under different pubertal development stages. Additionally, 200 participants with obesity (BMI >P95th) were matched with healthy children from the original cohort at a 1:1 ratio. All participants underwent bone mineral density assessment, and serum levels of P1NP and ß-CTX were measured. RESULTS: The BTMs values presented significant age, sex, and puberty stage differences. Analysis of serum BTMs based on the established reference revealed a higher percentage of low-level P1NP in boys with obesity (P=0.005); no significant difference was observed in girls. However, the obese group showed a significantly higher proportion of high ß-CTX levels for girls, not boys (P=0.022). CONCLUSIONS: We provide age-, sex-, and puberty stage-specific P1NP and ß-CTX reference curve. According to these, obesity appeared to be a negative factor for bone formation in boys and for bone resorption in girls.
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The C-F bond is the strongest covalent single bond (126 kcal/mol) in carbon-centered bonds, in which the highest electronegativity of fluorine (χ = 4) gives rise to the shortest bond length (1.38 Å) and the smallest van der Waals radius (rw = 1.47 Å), resulting in enormous challenges for activation and transformation. Herein, C-F conversion was realized via photouranium-catalyzed hydroxylation of unactivated aryl fluorides using water as a hydroxyl source to deliver multifunctional phenols under ambient conditions. The activation featured cascade sequences of single electron transfer (SET)/hydrogen atom transfer (HAT)/oxygen atom transfer (OAT), highly integrated from the excited uranyl cation. The *UO22+ prompted water splitting under mild photoexcitation, caging the active oxygen in a peroxo-bridged manner for the critical OAT process and releasing hydrogen via the HAT process.
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BACKGROUND: Postoperative pancreatic fistula (POPF) contributes significantly to morbidity and mortality after pancreaticoduodenectomy (PD). However, the underlying mechanisms remain unclear. This study explored this pathology in the pancreatic stumps and elucidated the mechanisms of POPF following PD. CASE SUMMARY: Pathological analysis and 16S rRNA gene sequencing were performed on specimens obtained from two patients who underwent complete pancreatectomy for grade C POPF after PD. Gradient inflammation is present in the pancreatic stump. The apoptosis was lower than that in the normal pancreas. Moreover, neutrophil-dominated inflammatory cells are concentrated in the ductal system. Notably, neutrophils migrated through the ductal wall in acinar duct metaplasia-formed ducts. Additionally, evidence indicates that gut microbes migrate from the digestive tract. Gradient inflammation occurs in pancreatic stumps after PD. CONCLUSION: The mechanisms underlying POPF include high biochemical activity in the pancreas, mechanical injury, and digestive reflux. To prevent POPF and address pancreatic inflammation and reflux, breaking the link with anastomotic dehiscence is practical.
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N,N-dimethylformamide (DMF) is a widely utilized chemical solvent with various industrial applications. Previous studies have indicated that the liver is the most susceptible target to DMF exposure, whereas the underlying mechanisms remain to be elucidated. This study aimed to investigate the role of NLRP3 inflammasome in DMF-induced liver injury in mice by using two NLRP3 inflammasome inhibitors, Nlrp3-/- mice, Nfe2l2-/- mice, and a macrophage-depleting agent. RNA sequencing revealed that endoplasmic reticulum (ER) stress and NLRP3 inflammasome-associated pathways were activated in the mouse liver after acute DMF exposure, which was validated by Western blotting. Interestingly, DMF-induced liver injury was effectively suppressed by two inflammasome inhibitors, MCC950 and Dapansutrile. In addition, knockout of Nlrp3 markedly attenuated DMF-induced liver injury without affecting the metabolism of DMF. Furthermore, silencing Nfe2l2 aggravated the liver injury and the NLRP3 inflammasome activation in mouse liver. Finally, the depletion of hepatic macrophages by clodronate liposomes significantly reduced the liver damage caused by DMF. These results suggest that NLRP3 inflammasome activation is the upstream molecular event in the development of acute liver injury induced by DMF.
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Dimetilformamida , Inflamassomos , Proteína 3 que Contém Domínio de Pirina da Família NLR , Animais , Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo , Proteína 3 que Contém Domínio de Pirina da Família NLR/genética , Camundongos , Inflamassomos/metabolismo , Doença Hepática Induzida por Substâncias e Drogas , Fígado/efeitos dos fármacos , Camundongos Knockout , Estresse do Retículo Endoplasmático/efeitos dos fármacosRESUMO
BACKGROUND: Aberrant expressions of desmoglein 2 (Dsg2) and desmocollin 2(Dsc2), the two most widely distributed desmosomal cadherins, have been found to play various roles in cancer in a context-dependent manner. Their specific roles on breast cancer (BC) and the potential mechanisms remain unclear. METHODS: The expressions of Dsg2 and Dsc2 in human BC tissues and cell lines were assessed by using bioinformatics analysis, immunohistochemistry and western blotting assays. Wound-healing and Transwell assays were performed to evaluate the cells' migration and invasion abilities. Plate colony-forming and MTT assays were used to examine the cells' capacity of proliferation. Mechanically, Dsg2 and Dsc2 knockdown-induced malignant behaviors were elucidated using western blotting assay as well as three inhibitors including MK2206 for AKT, PD98059 for ERK, and XAV-939 for ß-catenin. RESULTS: We found reduced expressions of Dsg2 and Dsc2 in human BC tissues and cell lines compared to normal counterparts. Furthermore, shRNA-mediated downregulation of Dsg2 and Dsc2 could significantly enhance cell proliferation, migration and invasion in triple-negative MDA-MB-231 and luminal MCF-7 BC cells. Mechanistically, EGFR activity was decreased but downstream AKT and ERK pathways were both activated maybe through other activated protein tyrosine kinases in shDsg2 and shDsc2 MDA-MB-231 cells since protein tyrosine kinases are key drivers of triple-negative BC survival. Additionally, AKT inhibitor treatment displayed much stronger capacity to abolish shDsg2 and shDsc2 induced progression compared to ERK inhibition, which was due to feedback activation of AKT pathway induced by ERK inhibition. In contrast, all of EGFR, AKT and ERK activities were attenuated, whereas ß-catenin was accumulated in shDsg2 and shDsc2 MCF-7 cells. These results indicate that EGFR-targeted therapy is not a good choice for BC patients with low Dsg2 or Dsc2 expression. Comparatively, AKT inhibitors may be more helpful to triple-negative BC patients with low Dsg2 or Dsc2 expression, while therapies targeting ß-catenin can be considered for luminal BC patients with low Dsg2 or Dsc2 expression. CONCLUSION: Our finding demonstrate that single knockdown of Dsg2 or Dsc2 could promote proliferation, motility and invasion in triple-negative MDA-MB-231 and luminal MCF-7 cells. Nevertheless, the underlying mechanisms were cellular context-specific and distinct.
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Movimento Celular , Proliferação de Células , Desmocolinas , Desmogleína 2 , Neoplasias de Mama Triplo Negativas , Humanos , Desmocolinas/metabolismo , Desmocolinas/genética , Desmogleína 2/metabolismo , Desmogleína 2/genética , Feminino , Neoplasias de Mama Triplo Negativas/metabolismo , Neoplasias de Mama Triplo Negativas/patologia , Neoplasias de Mama Triplo Negativas/genética , Linhagem Celular Tumoral , Neoplasias da Mama/metabolismo , Neoplasias da Mama/patologia , Neoplasias da Mama/genética , Invasividade Neoplásica , Regulação Neoplásica da Expressão Gênica , beta Catenina/metabolismo , Transdução de SinaisRESUMO
In light of the prevalent issues concerning the mechanical grading of fresh tea leaves, characterized by high damage rates and poor accuracy, as well as the limited grading precision through the integration of machine vision and machine learning (ML) algorithms, this study presents an innovative approach for classifying the quality grade of fresh tea leaves. This approach leverages an integration of image recognition and deep learning (DL) algorithm to accurately classify tea leaves' grades by identifying distinct bud and leaf combinations. The method begins by acquiring separate images of orderly scattered and randomly stacked fresh tea leaves. These images undergo data augmentation techniques, such as rotation, flipping, and contrast adjustment, to form the scattered and stacked tea leaves datasets. Subsequently, the YOLOv8x model was enhanced by Space pyramid pooling improvements (SPPCSPC) and the concentration-based attention module (CBAM). The established YOLOv8x-SPPCSPC-CBAM model is evaluated by comparing it with popular DL models, including Faster R-CNN, YOLOv5x, and YOLOv8x. The experimental findings reveal that the YOLOv8x-SPPCSPC-CBAM model delivers the most impressive results. For the scattered tea leaves, the mean average precision, precision, recall, and number of images processed per second rates of 98.2%, 95.8%, 96.7%, and 2.77, respectively, while for stacked tea leaves, they are 99.1%, 99.1%, 97.7% and 2.35, respectively. This study provides a robust framework for accurately classifying the quality grade of fresh tea leaves.
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Algoritmos , Aprendizado de Máquina , Rememoração Mental , Folhas de Planta , CháRESUMO
An increasing percentage of people in China are suffering from osteoporosis, particularly postmenopausal osteoporosis (PMOP), as the country rapidly evolves into an aging culture. Patients with osteoporosis are inclined to endure fractures, as well as deformities and impairments, which drastically decrease people's quality of life. The benefits of traditional Chinese medicine (TCM) treatment have continued to become increasingly apparent as reports of adverse responses to Western medications increased. The main advantage of traditional Chinese medicine treatment is that pharmacological interactions may be employed to lessen adverse effects while increasing therapeutic efficacy. In addition, there are various exercise therapies created by medical doctors in the past generations, such as: Wuqinxi, Taijiquan, Baduanjin, Yijinjing, etc. Chinese medicine and exercise treatment for postmenopausal osteoporosis have garnered a lot of attention recently both domestically and internationally, and investigations demonstrate that these therapies have considerable therapeutic effects. The pathophysiology of postmenopausal osteoporosis, advancements of herbal therapy options, and exercise treatment options are all thoroughly addressed in this article.
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Heart failure is the final stage of several cardiovascular diseases, and the key to effectively treating heart failure is to reverse or delay ventricular remodelling. Levosimendan is a novel inotropic and vasodilator agent used in heart failure, whereas the impact of levosimendan on ventricular remodelling is still unclear. This study aims to investigate the impact of levosimendan on ventricular remodelling in patients with left ventricular systolic dysfunction. Electronic databases were searched to identify eligible studies. A total of 66 randomized controlled trials involving 7968 patients were included. Meta-analysis results showed that levosimendan increased left ventricular ejection fraction [mean difference (MD) = 3.62, 95% confidence interval (CI) (2.88, 4.35), P < 0.00001] and stroke volume [MD = 6.59, 95% CI (3.22, 9.96), P = 0.0001] and significantly reduced left ventricular end-systolic volume [standard mean difference (SMD) = -0.52, 95% CI (-0.67, -0.37), P < 0.00001], left ventricular end-diastolic volume index [SMD = -1.24, 95% CI (-1.61, -0.86), P < 0.00001], and left ventricular end-systolic volume index [SMD = -1.06, 95% CI (-1.43, -0.70), P < 0.00001]. In terms of biomarkers, levosimendan significantly reduced the level of brain natriuretic peptide [SMD = -1.08, 95% CI (-1.60, -0.56), P < 0.0001], N-terminal pro-brain natriuretic peptide [SMD = -0.99, 95% CI (-1.41, -0.56), P < 0.00001], and interleukin-6 [SMD = -0.61, 95% CI (-0.86, -0.35), P < 0.00001]. Meanwhile, levosimendan may increase the incidence of hypotension [risk ratio (RR) = 1.24, 95% CI (1.12, 1.39), P < 0.0001], hypokalaemia [RR = 1.57, 95% CI (1.08, 2.28), P = 0.02], headache [RR = 1.89, 95% CI (1.50, 2.39), P < 0.00001], atrial fibrillation [RR = 1.31, 95% CI (1.12, 1.52), P = 0.0005], and premature ventricular complexes [RR = 1.86, 95% CI (1.27, 2.72), P = 0.001]. In addition, levosimendan reduced all-cause mortality [RR = 0.83, 95% CI (0.74, 0.94), P = 0.002]. In conclusion, our study found that levosimendan might reverse ventricular remodelling when applied in patients with left ventricular systolic dysfunction, especially in patients undergoing cardiac surgery, decompensated heart failure, and septic shock.
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Simendana , Disfunção Ventricular Esquerda , Remodelação Ventricular , Simendana/uso terapêutico , Simendana/farmacologia , Simendana/administração & dosagem , Humanos , Disfunção Ventricular Esquerda/tratamento farmacológico , Disfunção Ventricular Esquerda/fisiopatologia , Remodelação Ventricular/efeitos dos fármacos , Função Ventricular Esquerda/fisiologia , Função Ventricular Esquerda/efeitos dos fármacos , Volume Sistólico/fisiologia , Volume Sistólico/efeitos dos fármacos , Cardiotônicos/uso terapêutico , SístoleRESUMO
BACKGROUND: In clinical practice, stem cell transplantation has become an effective method for treating spinal cord nerve injury. Up to now, there has been no report on teratoma caused by transplanted stem cell's abnormal differentiation in the clinic, especially in the analysis of imaging manifestations. Therefore, this article aims to analyze the PET/CT imaging manifestations of teratoma caused by stem cell transplantation to improve the imaging diagnosing capability. CASE PRESENTATION: A patient with a spinal cord injury who had received a stem cell transplant was examined by PET/CT on September 10th, 2020. The PET/CT images of the lesion showed irregular mixed low density on the right side of the erector spinae muscle area at the level of the cervical 3-5 vertebral body, with a maximum cross-section of 9.1×3.9 cm. The 18F-FDG metabolism of the lesion was increased, and the maximum standard uptake value (SUVmax) was 10.7. The boundary was unclear with the third cervical vertebra and cervical 3 and 4-level vertebral plates. Based on the patient's medical history, the lesion was diagnosed as an abnormal proliferative tumor, which was consistent with the pathological examination results. CONCLUSION: To date, there have been no clinical reports on teratomas caused by stem cell transplantation for spinal cord injury at home or abroad. This case report enhances the knowledge of the diagnosis and treatment methods of this type of disease and confirms the diagnostic value of PET/CT examination.
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Traumatismos da Medula Espinal , Teratoma , Humanos , Tomografia por Emissão de Pósitrons combinada à Tomografia Computadorizada , Compostos Radiofarmacêuticos , Tomografia Computadorizada por Raios X/métodos , Teratoma/diagnóstico por imagem , Teratoma/cirurgia , Traumatismos da Medula Espinal/diagnóstico por imagem , Traumatismos da Medula Espinal/cirurgia , Transplante de Células-Tronco , Vértebras Cervicais/diagnóstico por imagem , Vértebras Cervicais/cirurgiaRESUMO
Although the SARS-CoV-2 pandemic has ended, multiple sporadic cases still exist, posing a request for more antivirals. The main protease (Mpro) of SARS-CoV-2, a key enzyme for viral replication, is an attractive target for drug development. Here, we report the discovery of a new potent α-ketoamide-containing Mpro inhibitor, N-((R)-1-cyclohexyl-2-(((R)-3-methoxy-1-oxo-1-((1-(2-oxo-2-((thiazol-2-ylmethyl)amino)acetyl)cyclobutyl)amino)propan-2-yl)amino)-2-oxoethyl)-4,4-difluorocyclohexane-1-carboxamide (20j). This compound presented promising enzymatic inhibitory activity against SARS-CoV-2 Mpro with an IC50 value of 19.0 nM, and an excellent antiviral activity in cell-based assay with an EC50 value of 138.1 nM. This novel covalent inhibitor may be used as a lead compound for subsequent drug discovery against SARS-CoV-2.
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COVID-19 , Proteases 3C de Coronavírus , SARS-CoV-2 , Humanos , Antivirais/farmacologia , Inibidores de Proteases/farmacologia , Simulação de Acoplamento MolecularRESUMO
Based on the ISAM module in the WRF-CMAQ model, this study analyzed the source contribution(both regional and sectoral) of O3 and its precursors(NO2 and VOCs) in Zibo in June 2021. Days with a maximum daily 8-h average(MDA8) O3 higher(lower) than 160 µg·m-3 were defined as polluted(clean) days. Differences in the source contribution between clean days and polluted days were compared, and a typical pollution period was selected for further process analysis. The results showed that NO2 in Zibo mainly came from local emissions in summer, with a relative contribution of 45.1%. Vehicle emissions(33.8%) and natural sources(20.7%) were the primary NO2 sources. VOC contributions from natural sources, solvent usage, and the petrochemical industry were significant, with a total contribution of 78.5%. The MDA8 contribution from local sources was 21.4%, whereas the impact of regional transport(32%) and surrounding cities(26.8%) was also substantial. Among local emission sources, vehicle emissions, the power industry, and the building materials industry contributed 10.9%-18.8% to local MDA8. On O3 pollution days, the MDA8 contribution from local emissions and surrounding cities increased. However, the relative contributions from local sources were similar under different pollution conditions.
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In large-scale seaweed farming, an understanding of the decomposition process plays a pivotal role in optimizing cultivation practices by considering the influence of the bacterial community. Therefore, we assessed the bacterial community structure and its influence on environmental factors during Gracilaria lemaneiformis decomposition, utilizing both microcosms and in-situ simulations. The decomposition rates in the microcosms and in situ simulations reached 79 % within 180 days and 81 % within 50 days, respectively In the microcosms, the dissolved oxygen content decreased from 5.3 to 0.4 mg/L, while the concentrations of total organic carbon, nitrogen, and phosphorus in the water increased by 165 %, 1636 %, and 2360 %, respectively. The common dominant bacteria included Proteobacteria, Planctomycetes, Firmicutes, Bacteroidetes, and Spirochaetae. Planctomycetes and Firmicutes were positively correlated with the total organic carbon, nitrogen, and phosphorus concentrations. Planctomycetes species played significant roles during the decomposition process. The overall findings of this study could inform more sustainable seaweed cultivation practices.
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Gracilaria , Rodófitas , Alga Marinha , Alga Marinha/química , Gracilaria/química , Bactérias , Firmicutes , Nitrogênio , Fósforo , CarbonoRESUMO
Background: Scutellaria amoena (SA) is the root of S. amoena C.H. Wright of Labiatae, also known as Scutellaria southwestern. This is mainly distributed in Sichuan, Yunnan, and Guizhou in China. In southwest China, SA is used as an alternative method to genuine medicine for the treatment of allergy, diarrhea, inflammation, hepatitis, and bronchitis. Thus far, studies on the effects of SA on non-alcoholic steatohepatitis (NASH) are lacking. This paper investigated the effect of SA on the regulation of gut microbiota and its metabolites in NASH rats by inhibiting the NOD-like receptor 3 (NLRP3)/apoptosis-associated speck-like protein (ASC)/caspase-1 axis. Methods: A NASH rat model was induced by a high-fat diet (HFD) for 12 weeks, and rats were orally given different doses of SA extracts (150 and 300 mg/kg/d) for 6 weeks. Changes in histological parameters, body weight, organ indexes, cytokines, and biochemical parameters related to NLRP3 in NASH rats were checked. 16S rRNA gene sequencing and UPLC-MS/MS technology were used to analyze the changes in the gut microbiota composition and its metabolites in NASH rats. Results: SA significantly inhibited the HFD-induced increase in body weight, lipid levels, and inflammatory infiltration. SA notably inhibited the HFD-induced increase in the upper and lower factors of NLRP3, such as transforming growth factor (TGF)-ß, tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-18, pro-IL-18, IL-1ß, pro-IL-1ß, NLRP3, ASC, and caspase-1. Additionally, mRNA expressions of caspase-1, NLRP3, and ASC were significantly downregulated after SA treatment. The results of the intestinal flora showed that SA could increase the diversity of flora and change its structure and composition in NASH rats by reducing Firmicutes/Bacteroidetes (F/B) ratio, Blautia (genus), Lachospiraceae (family), and Christensenellaceae R-7 group (genus), and increasing Muribaculaceae (family) and Bacteroides (genus). The metabolomics revealed that 24 metabolites were possibly the key metabolites for SA to regulate the metabolic balance of NASH rats, including chenodeoxycholic acid, xanthine, and 9-OxoODE. Nine metabolic pathways were identified, including primary bile acid biosynthesis, bile secretion, purine metabolism, and secondary bile acid biosynthesis. Conclusion: SA can regulate the intestinal microbial balance and metabolic disorder by inhibiting the NLRP3/ASC/caspase-1 axis to relieve NASH.