丹参酮ⅡA对马兜铃酸诱导的血管内皮细胞凋亡的保护作用及其可能机制  

Protective Effect of Tanshinone ⅡA on Apoptosis of Vascular Endothelial Cells Induced by Aristolochic Acid and Its Possible Mechanisms

作　　者：石红[1,2] 冯江敏[1] 邓婧宜[3] 

机构地区：[1]中国医科大学附属第一医院肾内科,辽宁省沈阳市110001 [2]抚顺市第二医院 [3]沈阳市第四人民医院

出　　处：《中国全科医学》2011年第11期1211-1214,共4页Chinese General Practice

摘　　要：目的探讨丹参酮ⅡA(TSN)对马兜铃酸(AA)诱导的血管内皮细胞凋亡的保护作用及其可能机制。方法不同浓度的TSN(0.2、0.4、0.8 mg/L)与人脐静脉血管内皮细胞(HUVECs)培养1 h后,加入10 mg/L的AA共同培养24 h。Hoechst 33258荧光染色观察细胞核的形态学改变,Annexin V-FITC/PI双染流式细胞仪检测细胞凋亡率,western blot法检测凋亡蛋白bcl-2和bax的表达及比色法测定caspase-3活性。结果与正常对照组相比,AA组细胞凋亡率显著增加,同时抗凋亡蛋白bcl-2的表达降低,促凋亡蛋白bax的表达及caspase-3活性均升高;而经TSN干预后,能逆转AA对细胞凋亡率、凋亡蛋白bcl-2和bax的表达及caspase-3活性的上述作用。结论 TSN可抑制AA诱导的血管内皮细胞凋亡,这可能与其促进抗凋亡蛋白bcl-2的表达、抑制促凋亡蛋白bax的表达和下调caspase-3活性有关。Objective To investigate the protective effect of tanshinone ⅡA（TSN） on the apoptosis of vascular endothelial cells stimulated by aristoloehic acid（AA） and its possible mechanisms.Methods Human umbilical vein endothelial cells（HUVECs） was cultured in TSN of different strength（0.2,0.4,0.8 mg/L） for 1h before 10 mg/L AA were added and incubated for another 24h.The nuclear morphological changes of apoptotic cells were observed through hoechst 33258 fluorescence staining.The proportions of apoptotic cells were assessed using flow cytometry.After 24h incubation,the expression levels of bcl-2 and bax were assessed with western blot.Meanwhile,the activity of caspase-3 was determined using colorimetric method.Results Compared with the control group,AA group showed an significantly increased proportion of apoptotic cells,a significant decrease in bcl-2 expression,and,significant increases in both bax expression and caspase-3 activity.All these changes were reversed after TSN intervention.Conclusion TSN can inhibit the apoptosis of endothelial cells induced by AA.The possible mechanism is：TSN can promote the expression of bcl-2,inhibit the expression of bax,and downregulate the activity of caspase-3.

关 键 词：丹参酮ⅡA 马兜铃酸 内皮细胞 凋亡 

分 类 号：R692.6[医药卫生—泌尿科学]