Effect of polydatin on miR-214 expression and liver function in ApoE-/- mice.
- Author:
Feng-Hua ZHOU
1
;
Zi-Yun WEN
;
Ze-Huai HE
;
Mei LI
;
Qiong-Li YIN
;
Cheng-Gang SHI
;
Cai-Lian CHENG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apolipoproteins E; genetics; Atherosclerosis; drug therapy; Blood Glucose; analysis; Diet, High-Fat; Disease Models, Animal; Drugs, Chinese Herbal; pharmacology; Glucosides; pharmacology; Lipids; blood; Liver; drug effects; Male; Malondialdehyde; metabolism; Mice; Mice, Inbred C57BL; Mice, Knockout; MicroRNAs; metabolism; Stilbenes; pharmacology; Superoxide Dismutase; metabolism
- From: Journal of Southern Medical University 2016;36(6):763-767
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effect of polydatin on the expression level of miR-214 and liver function in atherosclerotic mice.
METHODSForty male ApoE(-/-) mice were randomly allocated into 4 groups (n=10), namely the model group, low- and high-dose polydatin groups, and simvastin group, with 10 male C57BL/6J mice serving as the normal control group. Mouse models of atherosclerosis were established by feeding the ApoE(-/-) mice with a high-fat diet. After 12 weeks of treatment, blood levels of glucose, lipids, AST, and ALT and the contents of T-SOD and MDA in the liver tissue were detected. The pathologies of the liver were examined with HE staining, and miR-214 expression in the liver was detected using quantitative real-time PCR.
RESULTSCompared with the normal control mice, the mice in the model group showed significantly increased blood glucose, serum TC, TG, LDL-C, ALT, and AST levels, and MDA contents in the liver (P<0.01), with significantly decreased serum HDL-C level and SOD and miR-214 levels in liver (P<0.01). Polydatin treatment significantly ameliorated such changes in blood glucose, serum ALT, AST, TC, TG, LDL-C, and HDL-C levels, and MDA, SOD, and miR-214 contents in liver tissue (P<0.05).
CONCLUSIONs Polydatin can reduce blood glucose and lipid levels and protect the liver function in atherosclerotic mice possibly by up-regulating the expression of miR-214 and T-SOD and down-regulating MDA in the liver.