虎杖苷对ApoE-/-小鼠肝脏miR-214表达水平及肝功能的影响

目的研究虎杖苷（PD）对ApoE-/-小鼠肝脏miR-214及肝功能的影响。方法采用高脂饲料喂养雄性ApoE-/-小鼠，建立小鼠 AS模型。将ApoE-/-小鼠随机分为4组（n=10），即模型组（Model）、辛伐他汀组（Simvastatin）、PD低剂量组（PDL）、PD高剂量组 （PDH），另设10只同龄C57BL/6J小鼠为正常对照组。连续给药12周后取血，检测小鼠血糖、血脂、谷草转氨酶（AST）、谷丙转 氨酶（ALT）、肝脏T-SOD及MDA等指标，HE染色观察肝组织病理切片，实时荧光定量PCR检测miR-214水平。结果模型组小 鼠血糖和血清中TC、TG、LDL-C、ALT和AST，以及肝脏中MDA较正常对照组显著增高（P<0.01），血清中HDL-C和肝脏中 T-SOD、miR-214则显著降低（P<0.01），肝切片可见细胞内充满大小不一脂滴，大部分肝细胞呈现脂肪变性；与模型组相比，PD 高剂量组能显著降低小鼠空腹血糖、血清TC、TG、LDL-C、AST、ALT以及肝脏中的MDA（P<0.05），并且能够显著升高血清 HDL-C和肝脏miR-214及T-SOD（P<0.05）；PD高、低剂量组小鼠肝细胞脂肪变性与模型组相比均有所减轻。结论PD能降低 AS小鼠血糖、血脂，并保护肝功能，其机制可能主要与PD升高肝脏miR-214水平，调节T-SOD与MDA等氧化应激指标有关。

Effect of polydatin on miR-214 expression and liver function in ApoE-/-mice

Objective To study the effect of polydatin on the expression level of miR-214 and liver function in atherosclerotic mice. Methods 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. Results 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). 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.