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目的:探讨丹参酮ⅡA对心房颤动大鼠外周血金属基质蛋白酶(MMP-2/TIMP-2)和心房肌组织L型钙通道a1c亚单位(LTCCa1c)作用的影响,揭示直接的分子机制,为临床应用提供理论依据。方法:大鼠随机分成4组:正常对照组、模型组、丹参酮ⅡA治疗组和维拉帕米干预组。采用乙酰胆碱一氯化钙药物经尾静脉注射法构建房颤大鼠模型;用酶联免疫吸附试验检测大鼠血清MMP-2/TIMP-2表达变化;用免疫印迹法检测心房肌组织LTCCa1c蛋白表达变化。结果:与正常对照组相比,模型组外周血MMP-2水平明显增高、TIMP-2水平明显下降,LTCCa1c蛋白表达水平减低,两组比较具有差异性(P<0.05);与模型组相比,丹参酮ⅡA治疗组及维拉帕米干预组均降低MMP-2水平,升高TIMP-2水平,明显改善房颤大鼠心房肌组织LTCC蛋白表达水平减低状态(P<0.05)。结论:丹参酮ⅡA能够明显干预MMP-2/TIMP-2及LTCCa1c蛋白表达,显示可能通过多靶点作用,改善房颤大鼠心房肌组织重构过程的损伤程度,从而治疗房颤。
Objective: To investigate the effect of tanshinone ⅡA on the expression of matrix metalloproteinase-2 (MMP-2 / TIMP-2) and L-type calcium channel a1c subunit (LTCCa1c) in atrial fibrillation rats and to reveal the direct molecular mechanism. Application provides a theoretical basis. Methods: The rats were randomly divided into 4 groups: normal control group, model group, tanshinone Ⅱ A treatment group and verapamil intervention group. Atrial fibrillation rat model was established by intravenous injection of acetylcholine and calcium chloride via tail vein injection. The expression of MMP-2 / TIMP-2 in serum was detected by enzyme-linked immunosorbent assay (ELISA). The expression of LTCCa1c in atrial myocardium was detected by Western blotting Variety. Results: Compared with the normal control group, the levels of MMP-2 in the peripheral blood of model group were significantly increased, the level of TIMP-2 was significantly decreased and the expression of LTCCa1c protein was decreased in the model group (P <0.05). Compared with the model group , Tanshinone Ⅱ A treatment group and verapamil intervention group both decreased MMP-2 level, raised the level of TIMP-2 and ameliorated the decrease of LTCC protein expression in atrial fibrillation rats (P <0.05). Conclusion: Tanshinone Ⅱ A can significantly interfere with the expression of MMP-2 / TIMP-2 and LTCCa1c protein, indicating that it may be through multiple targets to improve atrial fibrillation rat atrial muscle remodeling process of injury, thus treating atrial fibrillation.