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1.
FASEB J ; 35(9): e21861, 2021 09.
Artigo em Inglês | MEDLINE | ID: mdl-34416029

RESUMO

Duchenne muscular dystrophy (DMD) is an intractable genetic disease associated with progressive skeletal muscle weakness and degeneration. Recently, it was reported that intraperitoneal injections of ketone bodies partially ameliorated muscular dystrophy by increasing satellite cell (SC) proliferation. Here, we evaluated whether a ketogenic diet (KD) with medium-chain triglycerides (MCT-KD) could alter genetically mutated DMD in model rats. We found that the MCT-KD significantly increased muscle strength and fiber diameter in these rats. The MCT-KD significantly suppressed the key features of DMD, namely, muscle necrosis, inflammation, and subsequent fibrosis. Immunocytochemical analysis revealed that the MCT-KD promoted the proliferation of muscle SCs, suggesting enhanced muscle regeneration. The muscle strength of DMD model rats fed with MCT-KD was significantly improved even at the age of 9 months. Our findings suggested that the MCT-KD ameliorates muscular dystrophy by inhibiting myonecrosis and promoting the proliferation of muscle SCs. As far as we can ascertain, this is the first study to apply a functional diet as therapy for DMD in experimental animals. Further studies are needed to elucidate the underlying mechanisms of the MCT-KD-induced improvement of DMD.


Assuntos
Dieta Cetogênica , Músculo Esquelético/efeitos dos fármacos , Músculo Esquelético/fisiologia , Distrofia Muscular de Duchenne/dietoterapia , Distrofia Muscular de Duchenne/fisiopatologia , Triglicerídeos/química , Triglicerídeos/farmacologia , Animais , Peso Corporal/efeitos dos fármacos , Proliferação de Células/efeitos dos fármacos , Modelos Animais de Doenças , Progressão da Doença , Feminino , Fibrose/dietoterapia , Fibrose/patologia , Inflamação/dietoterapia , Inflamação/patologia , Cetonas/sangue , Cetose , Masculino , Músculo Esquelético/patologia , Músculo Esquelético/fisiopatologia , Distrofia Muscular de Duchenne/patologia , Necrose/dietoterapia , Necrose/patologia , Ratos , Células Satélites de Músculo Esquelético/citologia , Células Satélites de Músculo Esquelético/efeitos dos fármacos , Triglicerídeos/uso terapêutico
2.
Pediatr Cardiol ; 41(1): 94-100, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31654097

RESUMO

The native T1 value at 3.0 Tesla is a sensitive marker of diffuse myocardial damage. We evaluated the clinical usefulness of native T1 mapping in symptomatic adults with congenital heart disease (CHD), particularly in the systemic right ventricle (RV). Prospectively, 45 consecutive symptomatic adults with CHD were enrolled: 20 with systemic RV and 25 with tetralogy of Fallot underwent cardiac magnetic resonance (CMR) imaging at 3.0 Tesla. The Modified Look-Locker Inversion recovery sequence was used for T1 mapping. Cardiovascular events in the systemic RV were defined as heart failure and tachyarrhythmia. Brain natriuretic peptide (BNP) and indexed systemic ventricular end-diastolic volume were significantly higher in the systemic RV group. The native T1 value and extracellular volume (ECV) of the septal and lateral walls were higher in the systemic RV group, suggesting high impairment of the myocardium in the systemic RV group. There was a strong correlation between the native T1 value and ECV of the septum (r = 0.58, P = 0.03) and lateral wall (r = 0.56, P = 0.046) in the systemic RV group. Seven patients with systemic RV had cardiovascular events. In univariate logistic regression analysis, BNP and native T1 values of the insertion point were important for predicting cardiovascular events. The native T1 value at 3.0 Tesla may be a sensitive, contrast-free, and non-invasive adjunct marker of myocardial damage in CHD and predictive of cardiovascular events in the systemic RV.


Assuntos
Fibrose/patologia , Cardiopatias Congênitas/fisiopatologia , Imageamento por Ressonância Magnética/métodos , Miocárdio/patologia , Adulto , Biomarcadores , Estudos de Casos e Controles , Feminino , Fibrose/dietoterapia , Cardiopatias Congênitas/complicações , Cardiopatias Congênitas/diagnóstico por imagem , Insuficiência Cardíaca/diagnóstico por imagem , Insuficiência Cardíaca/etiologia , Ventrículos do Coração/diagnóstico por imagem , Ventrículos do Coração/fisiopatologia , Humanos , Masculino , Pessoa de Meia-Idade , Valor Preditivo dos Testes , Estudos Retrospectivos
3.
BMC Complement Altern Med ; 19(1): 283, 2019 Oct 25.
Artigo em Inglês | MEDLINE | ID: mdl-31653214

RESUMO

BACKGROUND: A potato protein hydrolysate, APPH is a potential anti-obesity diet ingredient. Since, obesity leads to deterioration of liver function and associated liver diseases, in this study the effect of APPH on high fat diet (HFD) associated liver damages was investigated. METHODS: Six week old male hamsters were randomly separated to six groups (n = 8) as control, HFD (HFD fed obese), L-APPH (HFD + 15 mg/kg/day of APPH), M-APPH (HFD + 30 mg/kg/day), H-APPH (HFD + 75 mg/kg/day of APPH) and PB (HFD + 500 mg/kg/day of probucol). HFD fed hamsters were administered with APPH 50 days through oral gavage. The animals were euthanized and the number of apoptotic nuclei in liver tissue was determined by TUNEL staining and the extent of interstitial fibrosis was determined by Masson's trichrome staining. Modulation in the molecular events associated with apoptosis and fibrosis were elucidated from the western blotting analysis of the total protein extracts. RESULTS: Hamsters fed with high fat diet showed symptoms of liver damage as measured from serum markers like alanine aminotransferase and aspartate aminotransferase levels. However a 50 day long supplementation of APPH effectively ameliorated the effects of HFD. HFD also modulated the expression of survival and apoptosis proteins in the hamster liver. Further the HFD groups showed elevated levels of fibrosis markers in liver. The increase in fibrosis and apoptosis was correlated with the increase in the levels of phosphorylated extracellular signal-regulated kinases (pERK1/2) revealing a potential role of ERK in the HFD mediated liver damage. However APPH treatment reduced the effect of HFD on the apoptosis and fibrosis markers considerably and provided hepato-protection. CONCLUSION: APPH can therefore be considered as an efficient therapeutic agent to ameliorate high fat diet related liver damages.


Assuntos
Caspase 3/metabolismo , Metaloproteinase 2 da Matriz/metabolismo , Metaloproteinase 9 da Matriz/metabolismo , Obesidade/dietoterapia , Proteínas de Plantas/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Solanum tuberosum/metabolismo , Animais , Apoptose , Caspase 3/genética , Cricetinae , Dieta Hiperlipídica/efeitos adversos , Fibrose/dietoterapia , Fibrose/genética , Fibrose/metabolismo , Fibrose/fisiopatologia , Humanos , Fígado/citologia , Fígado/metabolismo , Fígado/patologia , Masculino , Metaloproteinase 2 da Matriz/genética , Metaloproteinase 9 da Matriz/genética , Mesocricetus , Obesidade/genética , Obesidade/metabolismo , Obesidade/fisiopatologia , Proteínas de Plantas/química , Hidrolisados de Proteína/química , Hidrolisados de Proteína/metabolismo , Proteínas Proto-Oncogênicas c-akt/genética , Solanum tuberosum/química
4.
Free Radic Biol Med ; 135: 60-67, 2019 05 01.
Artigo em Inglês | MEDLINE | ID: mdl-30818054

RESUMO

Food deprivation protects against ischemia-reperfusion (IR) injury through unknown mechanisms. In an experimental rat model of acute IR injury, we found that preoperative fasting for 3 days protects rats from tubular damage and renal functional decline by increasing antioxidant protection independently of the NF-E2-related factor 2 (Nrf2), and by maintaining mitochondrial morphology and function. In addition, further analysis revealed that fasting protects against tubulointerstitial fibrosis. In summary, our results point out to fasting as a robust nutritional intervention to limit oxidative stress and mitochondrial dysfunction in early acute kidney injury and also to promote long-term protection against fibrosis.


Assuntos
Injúria Renal Aguda/dietoterapia , Rim/metabolismo , Fator 2 Relacionado a NF-E2/genética , Traumatismo por Reperfusão/dietoterapia , Injúria Renal Aguda/genética , Injúria Renal Aguda/metabolismo , Injúria Renal Aguda/patologia , Animais , Antioxidantes/metabolismo , Jejum/metabolismo , Fibrose/dietoterapia , Fibrose/metabolismo , Fibrose/patologia , Privação de Alimentos , Humanos , Rim/lesões , Rim/patologia , Túbulos Renais/metabolismo , Túbulos Renais/patologia , Malondialdeído/metabolismo , Mitocôndrias/metabolismo , Fator 2 Relacionado a NF-E2/metabolismo , Estresse Oxidativo/genética , Ratos , Traumatismo por Reperfusão/genética , Traumatismo por Reperfusão/metabolismo , Traumatismo por Reperfusão/patologia
6.
Sci Rep ; 8(1): 10988, 2018 Jul 20.
Artigo em Inglês | MEDLINE | ID: mdl-30030497

RESUMO

Chronic kidney disease (CKD) poses a formidable challenge for public healthcare worldwide as vast majority of patients with CKD are also at risk of accelerated cardiovascular disease and death. Renal fibrosis is the common manifestation of CKD that usually leads to end-stage renal disease although the molecular events leading to chronic renal fibrosis and eventually chronic renal failure remain to be fully understood. Nonetheless, emerging evidence suggests that an aberrant activation of PI3Kγ signaling may play an important role in regulating profibrotic phenotypes. Here, we investigate whether a blockade of PI3Kγ signaling exerts any beneficial effect on alleviating kidney injury and renal fibrosis. Using a mouse model of angiotensin II (Ang II)-induced renal damage, we demonstrate that PI3Kγ inhibitor AS605240 effectively mitigates Ang II-induced increases in serum creatinine and blood urea nitrogen, renal interstitial collagen deposition, the accumulation of ECM proteins and the expression of α-Sma and fibrosis-related genes in vivo. Mechanistically, we reveal that AS605240 effectively inhibits Ang II-induced cell proliferation and phosphorylation of Akt in fibroblast cells. Furthermore, we demonstrate that Ang II-upregulated expression of IL-6, Tnf-α, IL-1ß and Tgf-ß1 is significantly attenuated in the mice treated with AS605240. Taken together, our results demonstrate that PI3Kγ may function as a critical mediator of Ang II-induced renal injury and fibrosis. It is thus conceivable that targeted inhibition of PI3Kγ signaling may constitute a novel therapeutic approach to the clinical management of renal fibrosis, renal hypertension and/or CKD.


Assuntos
Angiotensina II/efeitos adversos , Fibrose/dietoterapia , Inibidores de Fosfoinositídeo-3 Quinase , Insuficiência Renal Crônica/tratamento farmacológico , Insuficiência Renal Crônica/patologia , Animais , Proliferação de Células/efeitos dos fármacos , Classe Ib de Fosfatidilinositol 3-Quinase , Citocinas/metabolismo , Modelos Animais de Doenças , Fibroblastos/patologia , Rim/lesões , Camundongos , Fosforilação/efeitos dos fármacos , Quinoxalinas/uso terapêutico , Insuficiência Renal Crônica/induzido quimicamente , Tiazolidinedionas/uso terapêutico
7.
EBioMedicine ; 32: 172-181, 2018 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-29779700

RESUMO

Despite substantial declines in mortality following myocardial infarction (MI), subsequent left ventricular remodeling (LVRm) remains a significant long-term complication. Extracellular small non-coding RNAs (exRNAs) have been associated with cardiac inflammation and fibrosis and we hypothesized that they are associated with post-MI LVRm phenotypes. RNA sequencing of exRNAs was performed on plasma samples from patients with "beneficial" (decrease LVESVI ≥ 20%, n = 11) and "adverse" (increase LVESVI ≥ 15%, n = 11) LVRm. Selected differentially expressed exRNAs were validated by RT-qPCR (n = 331) and analyzed for their association with LVRm determined by cardiac MRI. Principal components of exRNAs were associated with LVRm phenotypes post-MI; specifically, LV mass, LV ejection fraction, LV end systolic volume index, and fibrosis. We then investigated the temporal regulation and cellular origin of exRNAs in murine and cell models and found that: 1) plasma and tissue miRNA expression was temporally regulated; 2) the majority of the miRNAs were increased acutely in tissue and at sub-acute or chronic time-points in plasma; 3) miRNA expression was cell-specific; and 4) cardiomyocytes release a subset of the identified miRNAs packaged in exosomes into culture media in response to hypoxia/reoxygenation. In conclusion, we find that plasma exRNAs are temporally regulated and are associated with measures of post-MI LVRm.


Assuntos
Ácidos Nucleicos Livres/sangue , Fibrose/dietoterapia , Óleos de Peixe/administração & dosagem , Infarto do Miocárdio/dietoterapia , Adulto , Idoso , Meios de Contraste/uso terapêutico , Feminino , Fibrose/sangue , Fibrose/diagnóstico por imagem , Fibrose/patologia , Humanos , Imageamento por Ressonância Magnética , Masculino , MicroRNAs/sangue , Pessoa de Meia-Idade , Infarto do Miocárdio/sangue , Infarto do Miocárdio/diagnóstico por imagem , Infarto do Miocárdio/patologia , Miócitos Cardíacos/efeitos dos fármacos , Pequeno RNA não Traduzido/genética , Volume Sistólico/genética , Função Ventricular Esquerda/genética , Remodelação Ventricular/efeitos dos fármacos
8.
Stem Cell Res ; 27: 65-73, 2018 03.
Artigo em Inglês | MEDLINE | ID: mdl-29331939

RESUMO

Volumetric muscle defect, caused by trauma or combat injuries, is a major health concern leading to severe morbidity. It is characterized by partial or full thickness loss of muscle and its bio-scaffold, resulting in extensive fibrosis and scar formation. Therefore, the ideal therapeutic option is to use stem cells combined with bio-scaffolds to restore muscle. For this purpose, muscle-derived stem cells (MDSCs) are a great candidate due to their unique multi-lineage differentiation potential. In this study, we evaluated the regeneration potential of MDSCs for muscle loss repair using a novel in situ fibrin gel casting. Muscle defect was created by a partial thickness wedge resection in the tibialis anterior (TA) muscles of NSG mice which created an average of 25% mass loss. If untreated, this defect leads to severe muscle fibrosis. Next, MDSCs were delivered using a novel in situ fibrin gel casting method. Our results demonstrated MDSCs are able to engraft and form new myofibers in the defect when casted along with fibrin gel. LacZ labeled MDSCs were able to differentiate efficiently into new myofibers and significantly increase muscle mass. This was also accompanied by significant reduction of fibrotic tissue in the engrafted muscles. Furthermore, transplanted cells also contributed to new vessel formation and satellite cell seeding. These results confirmed the therapeutic potential of MDSCs and feasibility of direct in situ casting of fibrin/MDSC mixture to repair muscle mass defects.


Assuntos
Fibrina/uso terapêutico , Músculo Esquelético/patologia , Células-Tronco/fisiologia , Animais , Diferenciação Celular/fisiologia , Células Cultivadas , Fibrose/dietoterapia , Fibrose/terapia , Camundongos , Músculo Esquelético/lesões , Regeneração , Células-Tronco/citologia
9.
PLoS One ; 12(9): e0185098, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-28934296

RESUMO

Systemic lupus erythematosus (SLE) is a disease that mostly affects women. Accelerated atherosclerosis is a high-risk factor associated with SLE patients. SLE associated with cardiovascular disease is one of the most important causes of death. In this study, we demonstrated that Lactobacillus paracasei GMNL-32 (GMNL-32), a probiotic species, exhibits anti-fibrosis and anti-apoptotic effects on the cardiac tissue of NZB/WF1 mice. Female NZB/W F1 mice, a well-known and commonly used lupus-prone mouse strain, were treated with or without GMNL-32 administration for 12 weeks. Oral administration of GMNL-32 to NZB/WF1 mice significantly increased the ventricular thickness when compared to that of NZB/WF1 mice. Administration of GMNL-32 significantly attenuated the cardiac cell apoptosis that was observed in exacerbate levels in the control NZB/WF1 mice. Further, the cellular morphology that was slightly distorted in the NZB/WF1 was effectively alleviated in the treatment group mice. In addition, GMNL-32 reduced the level of Fas death receptor-related pathway of apoptosis signaling and enhanced anti-apoptotic proteins. These results indicate that GMNL-32 exhibit an effective protective effect on cardiac cells of SLE mice. Thus, GMNL-32 may be a potential therapeutic strategy against SLE associated arthrosclerosis.


Assuntos
Lactobacillus paracasei , Lúpus Eritematoso Sistêmico/dietoterapia , Probióticos/administração & dosagem , Administração Oral , Animais , Apoptose/fisiologia , Western Blotting , Colágeno/metabolismo , Ciclo-Oxigenase 2/metabolismo , Modelos Animais de Doenças , Feminino , Fibrose/dietoterapia , Fibrose/metabolismo , Fibrose/patologia , Imunofluorescência , Ventrículos do Coração/metabolismo , Ventrículos do Coração/patologia , Marcação In Situ das Extremidades Cortadas , Lúpus Eritematoso Sistêmico/metabolismo , Lúpus Eritematoso Sistêmico/patologia , Metaloproteinase 9 da Matriz/metabolismo , Camundongos Endogâmicos NZB , Tamanho do Órgão , Distribuição Aleatória
10.
Andrology ; 5(5): 1023-1031, 2017 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-28743168

RESUMO

Calorie restriction (CR) refers to a reduction of calorie intake without compromising essential nutrients to avoid malnutrition. CR has been established as a non-genetic method of altering longevity and attenuating biological changes associated with aging. Aging is also an important risk factor for erectile dysfunction. The aim of this study was to examine whether CR diet can reverse the age-related alterations of erectile tissue in the aged rat. Four groups of rats were used: young rats (7 months) + ad libitum, aged rats (22 months) + ad libitum, young rats + CR diet, and aged rats + CR diet. The ad libitum group had free access to both food and water, and CR groups were fed 60% of the food intake of their ad libitum littermates, starting from 6 weeks before sacrifice. The penis was harvested and stained with antibodies to von Willebrand factor, smooth muscle α-actin, platelet-derived growth factor receptor-ß, phospho-eNOS, nNOS, and neurofilament. We also performed Masson trichrome staining and TUNEL assay. The blood samples were collected for the measurement of serum total testosterone level. The contents of endothelial cells, smooth muscle cells, pericytes, and neuronal cells as well as serum testosterone levels were significantly lower in the penis of aged rats than in their young littermates. CR significantly restored cavernous endothelial cells, smooth muscle cells, pericytes, and neuronal cell contents and decreased cavernous endothelial cell apoptosis and fibrosis in both young and aged rats. CR also increased serum testosterone level in aged rats, but not in young rats. CR successfully improved age-related derangements in penile neurovascular structures and hormonal disturbance. Along with a variety of lifestyle modifications, our study gave us a scientific rationale for CR as a non-pharmaceutical strategy to reprogram damaged erectile tissue toward neurovascular repair in aged men.


Assuntos
Envelhecimento , Restrição Calórica , Disfunção Erétil/dietoterapia , Pênis , Animais , Apoptose , Endotélio Vascular/patologia , Disfunção Erétil/sangue , Disfunção Erétil/patologia , Fibrose/dietoterapia , Masculino , Regeneração Nervosa , Óxido Nítrico Sintase Tipo III/metabolismo , Pênis/irrigação sanguínea , Pênis/inervação , Pênis/patologia , Fosforilação , Ratos , Testosterona/sangue
11.
Biomed Res Int ; 2017: 2418671, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-28546962

RESUMO

Curcumin, a polyphenol derived from the turmeric, has received attention as a potential treatment for renal fibrosis primarily because it is a relatively safe and inexpensive compound that contributes to kidney health. Here, we review the literatures on the applications of curcumin in resolving renal fibrosis in animal models and summarize the mechanisms of curcumin and its analogs (C66 and (1E,4E)-1,5-bis(2-bromophenyl) penta-1,4-dien-3-one(B06)) in preventing inflammatory molecules release and reducing the deposition of extracellular matrix at the priming and activation stage of renal fibrosis in animal models by consulting PubMed and Cnki databases over the past 15 years. Curcumin exerts antifibrotic effect through reducing inflammation related factors (MCP-1, NF-κB, TNF-α, IL-1ß, COX-2, and cav-1) and inducing the expression of anti-inflammation factors (HO-1, M6PRBP1, and NEDD4) as well as targeting TGF-ß/Smads, MAPK/ERK, and PPAR-γ pathways in animal models. As a food derived compound, curcumin is becoming a promising drug candidate for improving renal health.


Assuntos
Curcumina/uso terapêutico , Fibrose/prevenção & controle , Inflamação/prevenção & controle , Nefropatias/prevenção & controle , Animais , Fibrose/dietoterapia , Fibrose/genética , Fibrose/patologia , Humanos , Inflamação/dietoterapia , Inflamação/genética , Inflamação/patologia , Interleucina-1beta/genética , Rim/efeitos dos fármacos , Rim/patologia , Nefropatias/dietoterapia , Nefropatias/genética , Nefropatias/patologia , Modelos Animais , NF-kappa B/genética , Fator de Crescimento Transformador beta/genética
12.
Mol Nutr Food Res ; 61(3)2017 03.
Artigo em Inglês | MEDLINE | ID: mdl-27748993

RESUMO

SCOPE: Diabetic nephropathy (DN) is a major cause of end-stage renal disease. Here, we examined the effect of long-term consumption of a low-fat soy milk powder (LFSMP) on the diabetic kidney structure and function. METHODS AND RESULTS: KKAy mice were fed a casein-, LFSMP-, or high-fat soy mixture powder (HFSMP)-based diet for 4 months. Plasma and urine were subjected to a biochemical assay every 2-4 wk. Renal morphology and protein expression were evaluated by histochemical staining and western blots. Although HFSMP-based diet showed no protective effect on DN. LFSMP-fed mice exhibited lower water intake, urine output, and urinary albumin, and glucose excretion. Furthermore, strong preservation of renal structural proteins and low urinary N-acetyl-beta-d-glucosaminidase activity were observed in LFSMP-fed mice, indicating alleviation of renal injury. LFSMP-fed mice showed a lesser degree of mesangial matrix expansion, of tubulointerstitial fibrosis, and of myofibroblast differentiation. Finally, milder renal inflammation was found in LFSMP-fed mice, as evidenced by a decrease in urinary monocyte chemoattractant protein- 1 excretion and lesser macrophage infiltration into the tubulointerstitium. CONCLUSION: The present data suggests that long-term consumption of LFSMP but not HFSMP retards DN progression via suppressing renal injury, myofibroblast differentiation, and renal macrophage infiltration in diabetic condition.


Assuntos
Nefropatias Diabéticas/dietoterapia , Rim/efeitos dos fármacos , Nefrite/dietoterapia , Leite de Soja/farmacologia , Albuminúria/dietoterapia , Animais , Diabetes Mellitus Experimental/complicações , Diabetes Mellitus Tipo 2/complicações , Nefropatias Diabéticas/complicações , Nefropatias Diabéticas/fisiopatologia , Gorduras na Dieta/administração & dosagem , Fibrose/dietoterapia , Rim/patologia , Camundongos , Nefrite/patologia , Pós
13.
Nutrition ; 31(7-8): 923-30, 2015.
Artigo em Inglês | MEDLINE | ID: mdl-26059365

RESUMO

OBJECTIVES: Vitamin E is often used in the treatment of nonalcoholic fatty liver disease (NAFLD), including nonalcoholic steatohepatitis (NASH); however, the magnitude of treatment response associated with vitamin E in improving liver function and histology in NAFLD/NASH has not, to our knowledge, been quantified systematically. Thus, we conducted a meta-analysis of randomized controlled trials (RCTs) using vitamin E in the treatment of NAFLD/NASH. METHODS: PubMed, Medline, and Cochrane Library Full Text Database, and Japan Medical-Literature Database (Igaku Chuo Zasshi) were searched until March 2014, and five RCTs were identified for meta-analysis. RESULTS: According to a random effect model analysis of the five studies, vitamin E significantly reduced aspartate transaminase (AST) by -19.43 U/L, alanine aminotransferase (ALT) by -28.91 U/L, alkaline phosphatase (ALP) by -10.39 U/L, steatosis by -0.54 U/L, inflammation by -0.20 U/L, and hepatocellular ballooning by -0.34 U/L compared with the control group. Vitamin E treatment with NASH adult patients showed obvious reductions in not only AST of -13.91 U/L, ALT by -22.44 U/L, steatosis of -0.67 U/L, inflammation of -0.20 U/L, but also fibrosis of -0.30 U/L compared to the control treatment. CONCLUSIONS: Vitamin E significantly improved liver function and histologic changes in patients with NAFLD/NASH.


Assuntos
Hepatócitos/efeitos dos fármacos , Fígado/efeitos dos fármacos , Hepatopatia Gordurosa não Alcoólica/dietoterapia , Vitamina E/uso terapêutico , Alanina Transaminase/sangue , Fosfatase Alcalina/sangue , Antioxidantes/uso terapêutico , Aspartato Aminotransferases/sangue , Fígado Gorduroso/dietoterapia , Fibrose/dietoterapia , Hepatócitos/patologia , Humanos , Inflamação/dietoterapia , Fígado/enzimologia , Fígado/patologia , Hepatopatia Gordurosa não Alcoólica/sangue , Hepatopatia Gordurosa não Alcoólica/patologia , Ensaios Clínicos Controlados Aleatórios como Assunto , Resultado do Tratamento
15.
Food Chem Toxicol ; 52: 53-60, 2013 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-23123425

RESUMO

Dietary quercetin is highly abundant in edible plants, which possesses a wide range of pharmacological properties. This study was to investigate hepatoprotective effects of quercetin in the nonalcoholic steatohepatitis (NASH) gerbils induced by a high-fat diet (HFD), and to evaluate its regulatory mechanism on hepatic inflammatory response. The gerbils were fed with HFD for 28 days to induce NASH. From 15th day to 28th day, the treated drugs were given daily to each animal, respectively. The lipid profiles and biochemical markers were determined at the end of the experiment. The expressions of Sirt1, NF-κB p65 and iNOS were detected by immunohistochemistry and Western blot analysis. The results showed that oral administration of quercetin at doses of 30-60 mg/kg to hyperlipidemia rats for 14 days were highly effective in decreasing the levels of serum total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), alanine aminotransferase (ALT) and aspartate aminotransferase (AST). It could decrease lipid accumulation in the hepatocytes, and reduce serum levels of pro-inflammatory cytokines TNF-α and IL-6 via regulating the expressions of Sirt1, NF-κB p65 and iNOS. Thus, dietary quercetin had significant therapeutic benefits and could be explored as a potential promising candidate for the prevention of NASH.


Assuntos
Dieta Hiperlipídica/efeitos adversos , Fígado Gorduroso/dietoterapia , Fígado Gorduroso/etiologia , Quercetina/farmacologia , Administração Oral , Alanina Transaminase/sangue , Animais , Aspartato Aminotransferases/sangue , Colesterol/sangue , LDL-Colesterol/sangue , Suplementos Nutricionais , Modelos Animais de Doenças , Fígado Gorduroso/metabolismo , Fígado Gorduroso/patologia , Fibrose/dietoterapia , Gerbillinae , Hepatócitos/efeitos dos fármacos , Hepatócitos/metabolismo , Hiperlipidemias/dietoterapia , Hiperlipidemias/metabolismo , Interleucina-6/sangue , Fígado/efeitos dos fármacos , Fígado/metabolismo , Masculino , NF-kappa B/metabolismo , Óxido Nítrico Sintase Tipo II/sangue , Hepatopatia Gordurosa não Alcoólica , Quercetina/administração & dosagem , Ratos , Sirtuína 1/metabolismo , Triglicerídeos/sangue , Fator de Necrose Tumoral alfa/metabolismo
16.
Allergy ; 67(10): 1299-307, 2012 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-22913672

RESUMO

BACKGROUND: Fibrosis of the esophageal lamina propria is a known complication of eosinophilic esophagitis (EoE). To date, therapy with topical corticosteroids has been shown to reverse esophageal fibrosis in some patients; however, there is little evidence to suggest that dietary therapy can also reverse it. Our aim was to examine whether dietary therapy alone can reverse esophageal fibrosis in children with EoE. METHODS: We performed a historical cohort study based on children with EoE who had esophageal fibrosis on pretreatment biopsies using trichrome staining. Post-treatment biopsies were analyzed for fibrosis reversal, and results were compared between patients treated with dietary restriction and those that received topical steroids. Clinical characteristics (age, symptoms, duration of symptoms prior to therapy, treatment type, and duration of therapy) were recorded. Histological markers (eosinophil numbers and eosinophilic degranulation in both epithelium and lamina propria, basal zone hyperplasia, and the presence of eosinophilic microabscesses in the epithelium) were examined by reviewing hematoxylin and eosin-stained biopsies and by immunohistochemical staining. These were examined as potential predictors for fibrosis reversal. RESULTS: Fibrosis resolved following both dietary restriction and topical steroids (3/17 and 5/9 patients respectively, P = 0.078). Post-treatment symptom resolution and decreased intraepithelial eosinophil numbers were found to be the only significant predictors of fibrosis resolution. CONCLUSIONS: Dietary restriction alone, similar to topical steroids, can reverse fibrosis in children with EoE.


Assuntos
Esofagite Eosinofílica/complicações , Epitélio/patologia , Esôfago/patologia , Fibrose/dietoterapia , Fibrose/etiologia , Adolescente , Corticosteroides/uso terapêutico , Adulto , Criança , Pré-Escolar , Estudos de Coortes , Esofagite Eosinofílica/patologia , Feminino , Fibrose/patologia , Humanos , Masculino , Resultado do Tratamento , Adulto Jovem
17.
Nutr Clin Pract ; 25(3): 257-64, 2010 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-20581319

RESUMO

Protein calorie malnutrition (PCM) is a well-known complication of chronic liver disease (CLD). A major contribution to PCM in CLD is restriction of dietary protein intake. After many decades of injudicious reduction in dietary protein, cirrhotic patients are now prescribed appropriate amounts of protein. PCM in CLD is known to be associated with life-threatening complications. In the general approach to these patients, the initial and most important step for the clinician is to recognize the extent of malnutrition. Most patients tolerate a normal amount of dietary protein without developing hepatic encephalopathy (HE). Oral branched-chain amino acids (BCAAs) have a limited role in HE. Patients who exhibit dietary protein intolerance originally were thought to be best treated with BCAA formulations. Mixed evidence has been reported in multiple studies. In keeping with other reports, this article shows that in animal protein-intolerant patients, even those with advanced cirrhosis, vegetable protein-based diets are well tolerated. Another approach to management of apparent dietary intolerance is to optimize HE treatment with available medications. This article reviews the causes of HE, minimal HE, and PCM; examines nutrition requirements and assessment; and discusses treatment options for malnutrition in HE.


Assuntos
Aminoácidos/uso terapêutico , Proteínas na Dieta/uso terapêutico , Encefalopatia Hepática/dietoterapia , Desnutrição Proteico-Calórica/dietoterapia , Animais , Fibrose/dietoterapia , Encefalopatia Hepática/tratamento farmacológico , Encefalopatia Hepática/etiologia , Humanos , Hepatopatias/complicações , Hepatopatias/dietoterapia , Desnutrição Proteico-Calórica/etiologia
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