二苯乙烯苷通过核因子κB信号通路抑制过氧化氢诱导的人脐静脉内皮细胞凋亡  

Effects of 2,3,5,4′-Tetrahydroxystilbene-2-O-β-D-Glucoside on Apoptosis of HUVEC Induced by H_2O_2 and the Mechanism Involved NF-κB Signaling Pathway

作　　者：龙石银[1] 高细强[1] 张彩平[1] 乔新惠[1] 黄良珠[1] 佟丽[1] 陈武哲[1] 田英[1] 

机构地区：[1]南华大学生物化学与分子生物学教研室,湖南省衡阳市421001

出　　处：《中国动脉硬化杂志》2011年第6期479-482,共4页Chinese Journal of Arteriosclerosis

基　　金：国家自然科学基金(30800474)资助;湖南省科技厅项目(2008sk3072;2010SK3037;湘科条字[2009]130-19);湖南省教育厅项目(09C832);湖南省研究生创新项目(CX2010B385)资助

摘　　要：目的研究二苯乙烯苷对过氧化氢诱导人脐静脉内皮细胞凋亡的保护作用,探讨二苯乙烯苷是否通过核因子κB信号通路调节凋亡相关基因的表达来抑制细胞凋亡。方法体外培养人脐静脉内皮细胞,实验分为对照组、过氧化氢组和二苯乙烯苷组,采用显微镜观察细胞形态,MTT法检测细胞增殖率,流式细胞术检测细胞凋亡率,Western blot检测核因子κB p65、IκB、bcl-2蛋白的表达。结果过氧化氢能显著抑制内皮细胞增殖,增加细胞凋亡率;并增加核因子κB p65蛋白的表达,降低bcl-2和IκB蛋白的表达。二苯乙烯苷预处理后显著增加氧化损伤内皮细胞的增殖率,并降低细胞凋亡率;与过氧化氢组相比,二苯乙烯苷组核因子κB p65蛋白的表达显著降低,bcl-2和IκB蛋白的表达显著升高(P<0.01)。结论二苯乙烯苷对过氧化氢诱导人脐静脉内皮细胞凋亡具有保护作用,其机制可能与其抑制核因子κB/IκB信号通路并上调bcl-2蛋白的表达有关。Aim To investigate the protective effect of 2,3,5,4＇-tetrahydroxystilbene-2-O- β-D-glucoside （TSG） on human umbilical vein endothelial ceils （HUVEC） apoptosis induced by H202 and further explore whether this effect is related to the NF-KB signaling pathway and the exPression of apoptosis-related protein. Methods HUVEC were divided into three groups： control group, H2 02 group and TSG group. The proliferation and apoptosis rates of HUVEC were detected by MTF and flow cytometry respectively. The protein expression of NF-KB p65, IKB and bcl-2 were assessed by Western blot. Results According to the MTY and flow cytometry, the proliferation rate of HUVEC decreased significantly compared with control group （ P 〈 0. 01 ）, while the apoptosis rate increased obviously （ P 〈 0. 01 ） after treating with H2 02. The proliferation rate of TSG pretreatment group increased significantly （P 〈 0. O1 ） while the apoptosis rate decreased obviously （P 〈 0. 01 ） compared with H2 02 group. Compared with H2O2 group, Western blot analysis revealed that the expression of NF-KB p65 was declined and the level of IKB and bcl-2 were increased significantly after pretreated by TSG （P 〈 0. 01 ）. Conclusions TSG has a protective effect on the HUVEC apoptosis induced by H202 and this molecular mechanism may be associated with its inhibiting the activation of NF-KB/IKB signaling pathway and the up-regulating expression of bcl-2 protein.

关 键 词：二苯乙烯苷 人脐静脉内皮细胞 细胞凋亡 核因子κB/IκB信号通路 

分 类 号：R363[医药卫生—病理学]