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- W2360508214 abstract "Objective To investigate the antioxidative roles of clofibrate in kidneys of stroke-prone spontaneously hypertensive rats (SHRsp).Methods Ten rats were randomly divided into two groups (5 for each group),the clofibrate treated group which was fed with 0.25% clofibrate containing Funabashi SP diet (Funabashi,Japan) for 10 days,and the non-treatment group.The expression levels of mitochondrial Hydroxymethylglutaryl-CoA synthase (HMGCS2) and the phosphorylation levels of protein kinase B(Akt) were measured using immunoblotting analysis.The level of malondialdehyde (MDA),the activities of superoxide dismutase (SOD),catalase (CAT) and glutathione peroxidase (GSH-Px) were detected by respective assay kits.Results Clofibrate treatment significantly suppressed the MDA level [Clofibrate group:(0.21±0.02) vs SHRsp group (0.79±0.10) nmol/mg pro,P0.05],the activities of catalase [Clofibrate group (38.46±1.02) vs SHRsp group(46.65±3.52)U/mg pro,P0.05] and attenuated SOD [Clofibrate group (20.13±0.28) vs SHRsp group (22.59±0.90)NU/mg pro,P0.05].Although the non-treatment group showed higher GSH-Px activity than the clofibrate treatment group,the difference was not statistically significant.Clofibrate treatment notably increased the expression of renal HMGCS2 protein in SHRsp.No significant difference was detected for the level of total renal Akt in two groups,but the level of phosporylated Akt was significantly decreased in the clofibrate treatment group.Conclusion Clofibrate can reduce the renal oxidative stress in SHRsp through a non-antioxidant enzymatic pathway.An increased expression of renal HMGCS2 induced by clofibrate may be partially responsible for its antioxidative property." @default.
- W2360508214 created "2016-06-24" @default.
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- W2360508214 date "2010-01-01" @default.
- W2360508214 modified "2023-09-24" @default.
- W2360508214 title "The Possible Antioxidative Mechanisms of Clofibrate in Kidneys of Stroke-Prone Spontaneously Hypertensive Rats" @default.
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