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作 者:廖思聪 王大新[2] LIAO Sicong;WANG Daxin(Department of Cardiology,Xiangya Second Hospital,Central South University,Changsha 410011,China)
机构地区:[1]中南大学湘雅二医院心内科,长沙410011 [2]江苏省苏北人民医院心内科,江苏扬州225001
出 处:《实用医学杂志》2018年第14期2311-2315,2319,共6页The Journal of Practical Medicine
基 金:国家重大基础研究项目"973"计划(编号:2007CB936104);江苏省"六大人才高峰"项目(编号:2014-SWYY-052)
摘 要:目的探讨香烟烟雾暴露对小鼠血管平滑肌细胞凋亡的影响及分子机制,为防治动脉粥样硬化提供理论依据。方法香烟烟雾提取物体外干预小鼠血管平滑肌细胞,采用CCK-8法检测细胞增殖,Annexin V-FITC/PI流式细胞术分析细胞凋亡率,Western blot和real-time PCR分别检测Bcl-2、Bax、GRP78与Chop的蛋白和mRNA表达。结果相比对照组,香烟烟雾提取物处理组细胞增殖显著降低(P<0.05),细胞凋亡率呈浓度依赖性升高(P<0.01),Bcl-2蛋白与mRNA表达呈浓度依赖性下调(P<0.05),而Bax、GRP78与Chop的蛋白和mRNA表达则浓度依赖性上调(P<0.05)。结论香烟烟雾暴露可能通过内质网应激途径诱导VSMC凋亡。抑制VSMC凋亡可能是防治动脉粥样硬化新的研究思路。Objective To investigate the effect of cigarette smoke exposure on the apoptosis of vascular smooth muscle cells in mice and the possible mechanism so as to provide a theoretical basis for anti-atherosclerosis.Methods The murine vascular smooth muscle cells in vitro were treated with cigarette smoke extract(CSE).Cell proliferation was detected by CCK-8 assay.The apoptosis rate was analyzed by Annexin V-FITC/PI flow cytome-try.The expressed protein and mRNA of Bcl-2,Bax,GRP78 and chop were detected by Western Blot and real-time PCR,respectively.Results Compared with the control group,the cell proliferation of CSE-treated groups was significantly decreased(P<0.05),while the apoptotic rate of CSE-treated groups increased in a dose-de-pendent manner(P<0.01).The expression of Bcl-2 protein and mRNA was downregulated in the CSE-treated groups(P<0.05),while the protein and mRNA expression of Bax,GRP78 and Chop upreg-ulated in a concentra-tion dependent manner(P<0.05).Conclusion Cigarette smoke exposure induces VSMC apoptosis in vitro through endoplasmic reticulum stress pathway.Inhibition of VSMC apoptosis may be a new approach to anti-ath-erosclerosis.
关 键 词:血管平滑肌细胞 动脉粥样硬化 香烟烟雾提取物 凋亡
分 类 号:R543.5[医药卫生—心血管疾病]
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