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目的探讨活络效灵丹含药血清对乳鼠心肌细胞缺氧/复氧(H/R)损伤的保护作用及其机制。方法取体外培养的乳鼠心肌细胞,建立缺氧/复氧心肌细胞损伤模型。实验分为正常组、模型组(H/R组)、活络效灵丹拆方组和阳性药对照组(单硝酸异山梨酯组)。用MTT比色法检测活络效灵丹对H/R损伤心肌细胞存活率和细胞上清液中LDH漏出量的影响,优选活络效灵丹的最佳配伍组合,并测定各组细胞浆丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性;用RT-PCR法检测心肌细胞Bcl-2 mRNA、Bax mRNA的表达。结果实验优选出活络效灵丹全方、丹参当归配伍、丹参乳香配伍、丹参当归乳香配伍为最佳配伍。与正常组比较,模型组MDA含量升高、SOD活性降低(P<0.01),细胞Bcl-2 mRNA表达降低、Bax mRNA表达增高(P<0.01);与模型组比较,优选的活络效灵丹各配伍组胞浆SOD活性增高、胞浆MDA含量减少(P<0.01),心肌细胞Bax mRNA表达减少、Bcl-2 mRNA表达增高(P<0.01)。结论活络效灵丹对H/R损伤的心肌细胞具有保护作用,其作用机制可能与清除氧自由基、抗脂质过氧化、上调Bcl-2 mRNA和下调Bax mRNA表达等有关。
Objective To investigate the protective effect and mechanism of Hailinglinglingdan containing serum on hypoxia / reoxygenation (H / R) injury of neonatal rat cardiomyocytes. Methods The neonatal rat cardiomyocytes were isolated and cultured to establish hypoxia / reoxygenation cardiomyocyte injury model. The experiment was divided into normal group, model group (H / R group), active Xiaoningdan decoction group and positive drug control group (isosorbide mononitrate group). MTT assay was used to detect the effect of Huaxiaolongdan on H / R-injured cardiomyocytes and LDH leakage in the cell supernatant. The best compatibility combination of Huaxiaolongdan was selected, (MDA) content and superoxide dismutase (SOD) activity. The expressions of Bcl-2 mRNA and Bax mRNA in cardiomyocytes were detected by RT-PCR. The results of the experiment selected active all active Dan Dan, Salvia Angelica compatibility, compatibility of Salvia miltiorrhiza, Salvia Angelicae sinensis compatibility best compatibility. Compared with the normal group, the content of MDA in the model group increased, the activity of SOD decreased (P <0.01), the expression of Bcl-2 mRNA decreased and the expression of Bax mRNA increased (P <0.01). Compared with the model group, The activity of SOD in the cytoplasm increased and the content of MDA in cytoplasm decreased (P <0.01). The expression of Bax mRNA and Bcl-2 mRNA in cardiomyocytes increased (P <0.01). Conclusion Active Ling Ling Dan has a protective effect on H / R injured cardiomyocytes. Its mechanism may be related to scavenging oxygen free radicals, anti-lipid peroxidation, up-regulating Bcl-2 mRNA and down-regulating Bax mRNA expression.