黄芪注射液对内皮细胞损伤的保护效应

PROTECTIVE EFFECTS OF ASTRAGALUS MEMBRANACEUS INJECTION ON ENDOTHELIAL CELL INJURY

目的 了解黄芪注射液对内皮细胞损伤的保护作用及其机制。方法 人脐静脉内皮细胞原代培养，传至3代后，分为3组。对照组：常规培养；低氧复氧组：先低氧处理1h，再复氧1h；药物干预组：在培养液中加入终浓度分别为5、10、20、40、60mg／L的黄芪注射液，12h后进行低氧复氧处理。测定各组细胞上清液中乳酸脱氢酶（LDH）活性、超氧化物歧化酶（SOD）活性和丙二醛（MDA）含量，检测内皮细胞台盼蓝摄取率。结果低氧复氧组与对照组比较．细胞培养液中LDH活性、MDA含量及内皮细胞台盼蓝摄取率升高，SOD活性减低，差异均有显著性（F=34．97～129．98，q=14．43～27．11，P〈0．01）。药物干预组与低氧复氧组比较，细胞培养液中LDH活性、MDA含量及内皮细胞台盼蓝摄取率降低，SOD活性升高，差异均有显著性（q=2．91～26．61，P〈0．05、0．01）。黄芪注射液预处理浓度为40mg／L时LDH活性、SOD活性、MDA含量与对照组比较差异无显著性（q=0．49～0．94，P〉0．05）；黄芪注射液预处理浓度60mg／L与40mg／L相比，LDH活性、SOD活性、MDA含量变化均不明显。结论 低氧复氧过程造成内皮细胞脂质过氧化损伤，细胞死亡率增加。黄芪注射液可能通过抗脂质过氧化，对低氧复氧内皮细胞产生保护作用。

Objective To investigate the protective effects of Astragal.us Membranaceus Injection （AMI） on endothelial. cell injury and its mechanism. Methods Human umbilical venous endothelial cells （HUVECs） were primarily cultured, passed down to the third generation, and then divided into three groups. Control group： the cells were conventionally cultured; hypoxia/ re oxygenation group： the cells were treated with hypoxia （1 h） and then re-oxygenation （1 h）; AMI group： different doses of AMI （5, 10. 20, 10. 60 mg/L） were added into the culture medium, and hypoxia/re-oxygenation was managed 12 hours later. The activity of I.DH and superoxide dismutase （SOD）, content of malondialdehyde （MDA） in cell medium were determined. The up-take rate of trypan-blue in each group was detected. Results In hypoxia/reoxygenation group, the activity of LDH, the con tent of MDA, and the uptake rate of trypan-blue were higher, and the activity of SOD was lower than the control group, the differences were significant （F=34.97-129.98, q=14.43-27. 11, P〈0.01）. In AMI group, the activity of I.DH, the content of MDA ,and the up-take rate of trypan blue decreased, and SOD activity increased as compared with hypoxia/reoxygenation group, the differences were significant （q= 2. 91 -26. 61; P〈0. 05,0. 011. When the pretreatment concentration of AMI was 40 g/i., the differences between AMI group and control group were not significant in terms of I.DH, SOD and MDA （q=0.49- 0,94, P〉0.05）. The changes of LDH, SOD and MDA, when the concentrations of AMI were 60 g/L and 40 g/L, were not marked. Conclusion Hypoxia/re oxygenation could injure HUVECs correlated with lipid peroxides and lead to endothelial cell death. Astragalus Membranaceus Injection can protect the cell damage caused by hypoxia reoxygenation process via antioxidant effect of lipids.