Effect of polydatin on miR-214 expression and liver function in ApoE-/- mice / 南方医科大学学报
Journal of Southern Medical University
;
(12): 763-767, 2016.
Artigo
em Chinês
| WPRIM
| ID: wpr-286902
ABSTRACT
<p><b>OBJECTIVE</b>To study the effect of polydatin on the expression level of miR-214 and liver function in atherosclerotic mice.</p><p><b>METHODS</b>Forty 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.</p><p><b>RESULTS</b>Compared 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).</p><p><b>CONCLUSION</b>s 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.</p>
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Apolipoproteínas E
/
Farmacologia
/
Estilbenos
/
Superóxido Dismutase
/
Sangue
/
Glicemia
/
Medicamentos de Ervas Chinesas
/
Camundongos Knockout
/
MicroRNAs
/
Modelos Animais de Doenças
Limite:
Animais
Idioma:
Chinês
Revista:
Journal of Southern Medical University
Ano de publicação:
2016
Tipo de documento:
Artigo
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