当归超滤物抗阿霉素致心肌细胞损伤的作用研究

目的探讨当归超滤物抗阿霉素致乳鼠心肌细胞损伤的作用及其可能机制。方法用阿霉素诱导Wistar乳鼠原代培养的心肌细胞建立损伤模型，用不同浓度的当归超滤物进行干预，实验分为正常对照组、阿霉素损伤模型组、当归超滤物不同浓度（3．75、7．5、15g／L）干预组。四氮唑蓝（MTT）法检测各组心肌细胞的存活率，2，4二硝基苯肼显色法检测各组细胞培养上清液中乳酸脱氢酶（LDH）的含量，Ca2＋-ATP酶试剂盒测定Ca2＋-ATP酶活性，蛋白印迹半定量测定各组细胞内caspase-3、caspase-12蛋白的表达。结果与阿霉素损伤模型组比较，当归超滤物各干预组心肌细胞存活率明显升高，LDH含量显著降低（P〈0．05），Ca2＋-ATP酶活性显著提高（P〈0．05），caspase-3、caspase-12表达显著降低（P〈0．05）。结论当归超滤物具有拮抗阿霉素致心肌细胞损伤的作用，其机制与其增强细胞ATP酶活性、降低细胞内LDH释放、抑制凋亡因子释放有关。

Study on the Effect of Angelica Eextract on Ultrafiltration Membrane on Adriamycin Damage in Cardiomyocytes

Objective To investigate whether the administration of the angelica extract on ultrafiltration membrane able to protect cardiomyocytes from adriamycin injury of rats and its potential mechanism. Methods Myocardial cells from 2 to 3days neonatal rats were cultured in DF medium and the cellular injury was induced by adriamycin. The angelica extract on uhrafiltration membrane was given in different concentrations. The experiments were divided into normal control group, adriamycin damage model group and medicine of different concentrations intervention group. Survival rate of myocardial cells was assessed by MTT,and the release of lactate dehydrogenase （LDH） in culture medium was evaluated by means of 2,4 dinitro -phenylhydrazine colorimetric reaction. Ca2＋ -atpase release quantity was using Ca2＋ - atpase kit methods detected, caspase - 3, caspase - 12 proteins were observed and determined with immunohistochemical western blot method. Results The angelica extract on uhrafihration membrane could protect the cardiomyocytes from adriamycin injury, decrease LDH （P 〈 0.05 ） , increase Ca2＋- atpase activity （ P 〈 0.05 ） , and downregulate caspase - 3, caspase - 12 proteins expression （ P 〈 0.05）. Conclusion The angelica extract on ultrafihration membrane has protection on cardiomyocytes injured by adriamycin through im- proving cell atpase content, reducing the intracellular LDH release and inhibiting apoptosis related factor release.