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1.
Journal of Clinical Hepatology ; (12): 1545-1550, 2020.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-822899

RESUMO

@# ObjectiveTo investigate the clinical effect of vitamin E in the treatment of nonalcoholic fatty liver disease (NAFLD) in children. MethodsPubMed, Web of Science, The Cochran Library, Embase, OVID/NEJM, CNKI, and Wanfang Data were searched for the articles on vitamin E in the treatment of NAFLD in children published up to December 2019. The data of 8 parameters were analyzed, i.e., body mass index (BMI), liver enzymes [alanine aminotransferase (ALT) and aspartate aminotransferase (AST)], blood lipid levels [triglyceride (TG), total cholesterol (TC), low-density lipoprotein (LDL), and high-density lipoprotein (HDL)], and remission rate of hepatic steatosis. RevMan 5.3 was used to perform a Meta-analysis. Continuous variables were analyzed by standardized mean difference (SMD) and 95% confidence interval (CI), and the changes after intervention were analyzed; categorical variables were analyzed by risk difference (RD) and 95%CI. A fixed effects model was used for homogeneous data, and a random effects model was used for heterogeneous data. Funnel plots were used to evaluate publication bias. ResultsA total of 599 articles were retrieved, among which 9 were included in the Meta-analysis, with 607 subjects in total. Vitamin E significantly improved the level of ALT (SMD = -0.27, 95%CI: -0.48 to -0.06, P=0.01), but it did not improve the levels of BMI (SMD=-0.09, 95%CI: -0.28 to 0.10, P=0.34), AST (SMD=-020, 95%CI: -0.42 to 0.02, P=0.07), TG (SMD=-0.19, 95%CI: -0.51 to 0.12, P=0.22), TCHO (SMD=-0.11, 95%CI: -0.31 to 0.08, P=0.24), HDL (SMD=-0.02, 95%CI: -0.27 to 0.23, P=0.88), LDL (SMD= -0.04, 95%CI: -0.27 to 019, P=072), and the remission rate of hepatic steatosis (RD=0.06, 95%CI: -0.05 to 0.17, P=0.29). ConclusionVitamin E can significantly improve the level of ALT in children with NAFLD and can be considered as an adjuvant drug for clinical treatment.

2.
Chongqing Medicine ; (36): 3464-3467, 2014.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-453991

RESUMO

Objective To investigate the effect of astaxanthin on the peripheral blood endothelial progenitor cells (EPCs) apop-tosis induced by oxidative stress in vitro and to explore its underlying mechanism .Methods Human peripheral blood EPCs were in vitro cultured and divided into the control group ,model group with 100 μmol/L tert-butyl hydroperoxide(tBHP) and the astaxan-thin plus tBHP group(with 0 .10 ,1 .00 ,10 .00 nmol/L astaxanthin pretreatment for 24 h ,then adding the final concentration of 100μmol/L tBHP for 6 h continuous culture) .The cell viability was measured by the MTT method .The level of reactive oxygen spe-cies (ROS) was determined by the DCFH-DA method .The changes of mitochondrial membrane potential(MMP) and the apoptosis ratio were detected by the JC-1 method and the DAPI method ,respectively .Results Compared with control group ,100μmol/L tB-HP could obviously caused the apoptosis of EPCs(P<0 .05) ,while astaxanthin could decrease tBHP induced apoptosis ,which man-ifested by the decrease of the apoptosis ratio (P<0 .05) and MMP increase .Conclusion Astaxanthin has the protective effect on the apoptosis of EPCs ,its mechanism may be related with the protection of the mitochondrial function .

3.
Acta Histochem Cytochem ; 41(5): 127-33, 2008 Oct 29.
Artigo em Inglês | MEDLINE | ID: mdl-18989466

RESUMO

To visualize completely rat retinal microvessels, the gelatin-ink perfusion condition was systematically optimized using von Willebrand factor (vWf) immunostaining as control. Whether the vessel showed by the new perfusion condition can be used for double label with neurons or glial cells in the same retina was also tested. Our results showed that infusing rats first with 20 ml of 37 degrees C ink plus 3% gelatin at 140% rat mean arterial pressure (MAP), and subsequently with 20 ml of 37 degrees C ink plus 5% gelatin at 180% rat MAP allowed the ink to completely fill the rat retinal microvessels. Rat retinal microvessels labeled by the perfusion method were more in number than that by vWf immunostaining. Moreover, our data, for the first time, displayed that the improved gelatin-ink perfusion had no effect on and caused no contamination to the following fluorogold labeling or immunostaining of retinal neurons or glial cells in the same tissue. These data suggest that the improved gelatin-ink perfusion technique is a superior method for morphological characterization of rat retinal microvessels, compatible to the double labeling of glial cells and neurons, and it extends the practical scale of the classic method.

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