摘要:
Objective To investigate the protective effects and mechanisms of SSTF on human umbilical vascular endothelial cells (HUVEC) following oxidative injury caused by hydrogen peroxide (H2O2).Methods On the basis of oxidative injury model of HUVEC,the cell vitality (OD value) was measured by MTT,MDA content,LDH activity,SOD activity of each group were measured by the method of biochemical assay,apoptosis ratio of each group was checked by FCM,and inhibition apoptosis protein Bcl-2 of each group were measured by the method of western-blot.Results When HUVEC were injured by H2O2,the cell vitality (OD value) and the activity of SOD declined,while the activity of LDH,the content of MDA,and the apoptosis ratio of HUVEC increased (P < 0.05 or P <0.01).The SSTF (100-400 mg/L) significantly increased the cell vitality (OD value),inhibited activity of LDH,decreased the content of MDA,increased the activity of SOD,decreased the apoptosis rate of HUVEC injured by H2O2,and improved the level of Bcl-2 (P < 0.05 or P < 0.01).Conclusion The SSTF can ease the injury of HUVEC,and decrease the apoptosis of HUVEC injured by H2O2.The mechanism may concern that it can improve the level of Bcl-2 to inhibit the apoptosis of HUVEC.%目的 探讨黄芩茎叶总黄酮(SSTF)对过氧化氢(H2O2)所致人脐静脉内皮细胞(HUVEC)氧化损伤的保护作用及其可能机制.方法 在由H2O2制备血管内皮细胞氧化损伤模型的基础上,采用MTT法测定各组细胞活力;生化比色法测定各组细胞培养上清液中乳酸脱氢酶(LDH)的活性,丙二醛(MDA)的含量及超氧化物歧化酶(SOD)的活性;流式细胞术检测各组细胞的凋亡率以及western-blot法测定各组细胞凋亡抑制蛋白Bcl-2的表达情况.结果 H2O2处理HUVEC后其存活率较正常HUVEC下降,细胞培养上清液中LDH活性和MDA含量明显增加,SOD活性较正常HUVEC降低;HUVEC凋亡率明显升高(P<0.05或P<0.01);而SSTF(100 ~400 mg/L)各剂量都能提高H2O2损伤的HUVCE的细胞活力,明显降低LDH活性,显著减少MDA的含量,提高SOD的活性,明显降低HUVEC凋亡率,明显提高Bcl-2蛋白表达水平(P<0.05或P<0.01).结论 SSTF能减轻H2O2对HUVEC的氧化损伤作用,降低H2O2所致HUVEC的凋亡率,其机制可能与上调凋亡抑制蛋白Bcl-2的表达水平有关.