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目的:探讨麝香保心丸和吡格列酮对代谢综合征(MS)大鼠心肌NF-κB、PPAR-α和PPAR-γ表达的影响。方法:60只大鼠随机分为空白对照组(A组)和MS模型组(B组),构建MS模型后将B组余下大鼠随机分为模型对照组(B1组)、麝香保心丸组(B2组,麝香保心丸13.5 mg·kg-1·d-1)、吡格列酮组(B3组,吡格列酮1.5 mg·kg-1·d-1)、麝香保心丸+吡格列酮组(B4组,麝香保心丸13.5 mg·kg-1·d-1+吡格列酮1.5 mg·kg-1·d-1)。比较不同药物干预对大鼠收缩压、血脂、血糖、空腹胰岛素(FINS)以及大鼠心肌组织NF-κB、PPAR-α和PPAR-γ表达的影响。结果:造模后B组大鼠收缩压、血脂、血糖及FINS较A组升高(P<0.05,P<0.01)。药物干预后,B2、B3、B4组收缩压、血脂、血糖及FINS较B1组改善(P<0.05,P<0.01),且B4组改善情况较B2、B3组更明显(P<0.05)。与B1组相比,B2、B3、B4组大鼠心肌组织NF-κB表达下调,PPAR-α、PPAR-γ表达增加(P<0.05),这种调控在B4组更明显(P<0.05)。结论:麝香保心丸和吡格列酮均可调控MS大鼠心肌NF-κB、PPAR-α和PPAR-γ的表达,改善MS大鼠心肌重构,两者合用时影响更明显。
Objective: To investigate the effects of Shexiang Baoxin Pills and pioglitazone on the expression of NF-κB, PPAR-α and PPAR-γ in myocardium of rats with metabolic syndrome. Methods: Sixty rats were randomly divided into blank control group (group A) and MS model group (group B). After establishing MS model, the remaining rats in group B were randomly divided into model group (group B1), musk pill (B2 group, 13.5 mg · kg -1 · d -1 of musk pill, group B3, 1.5 mg · kg -1 · d -1 pioglitazone, group B4 , Shexiang Baoxin Pill (13.5 mg · kg -1 · d -1) and pioglitazone (1.5 mg · kg -1 · d -1). The effects of different drugs on systolic blood pressure, blood lipid, blood glucose, fasting insulin (FINS) and the expression of NF-κB, PPAR-α and PPAR-γ in rat myocardium were compared. Results: After modeling, systolic blood pressure, blood lipid, blood glucose and FINS in group B were significantly higher than those in group A (P <0.05, P <0.01). After intervention, the systolic blood pressure, blood lipid, blood glucose and FINS in group B2, B3 and B4 were significantly improved compared with group B1 (P <0.05, P <0.01), and the improvement in group B4 was more obvious than that in group B2 and B3 (P <0.05). Compared with B1 group, the expression of NF-κB and PPAR-α and PPAR-γ in myocardium of B2, B3 and B4 groups were decreased (P <0.05), which was more obvious in B4 group (P <0.05) . CONCLUSION: Both Shexiang Baoxin Pill and pioglitazone can regulate the expression of NF-κB, PPAR-α and PPAR-γ in myocardium of MS rats and improve myocardial remodeling in MS rats.