中文摘要：

目的研究中药黄芩苷（baicalin，Bai）对羟自由基致大鼠乳鼠心肌细胞损伤的保护作用。方法原代SD大鼠乳鼠心肌细胞培养，48小时后加入Fe^2＋和半胱氨酸产生羟自由基造成心肌细胞损伤，损伤前30分钟加入不同浓度的黄芩苷作为保护剂。24小时后甲基四唑兰（MTT）法测定心肌细胞活性；试剂盒测定培养液中乳酸脱氢酶（LDH）活力、心肌细胞中脂质过氧化产物丙二醛（MDA）含量、超氧化物歧化酶（SOD）活性；并应用原位末端标记法（TUNEL）标记细胞后应用流式细胞仪测定细胞凋亡率。结果Fe^2＋和半胱氨酸能明显造成心肌细胞损伤，表现为：细胞活性下降、LDH活性增加、MDA含量增加、SOD活力下降；流式细胞仪显示细胞凋亡率增高。黄芩苷4．5μmol／L、9μmol／L、18μmol／L对损伤心肌细胞有保护作用，使结果受损程度有所改善，并随浓度增加保护作用加强。结论黄芩苷能减轻羟自由基对心肌细胞的损伤作用，降低羟自由基导致培养心肌细胞损伤的凋亡率。

英文摘要：

Objective To investigate the protective function of baicalin, which was observed in freshly isolated myocardial cell damaged by Fe^2＋/cysteine. Methods Culture cardiac mycyte were incubated with Fe^2＋/Cys system for 24 hours. And 30 minutes before, give baicalin as protective agent. Assay the activity of myocardial cell by MTT. The activity of LDH was determined by Beckman CX5pro machine. The content of MDA and activity of SOD in cell were determind by MDA and SOD kit. Flow cytometry detect the rate of apoptosis . Rnsults Fe^2＋/cysteine could induce obvious oxidative injure on cultured cardiac myocyte . It was found the descend of livability, the activity of LDH in culture medium and the content of MDA increase and activity of SOD decrease. Different concentration baicalin （4.5μmol/L、9μmol/L、18μmol/L） can protect the injure cell , and the protective effect increase with the rise of concentration. Conclusions Baicalin can ease the injury of cardiac myocyto which were disposed by hydroxide , and the mechanism maybe respect with it＇ s effect of chock back surcharge of calcium .