异丙酚对缺氧复氧损伤人血管内皮细胞caspase-3和Bcl-2蛋白表达的影响研究
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- 论文作者：阮志华 ; 郑晓明
- 年：2016
- 作者机构：十堰市太和医院(湖北医药学院附属医院)麻醉科;十堰市太和医院(湖北医药学院附属医院)中心手术室;
- 论文关键词：异丙酚 ; 缺氧复氧 ; 内皮细胞 ; caspase-3 ; Bcl-2
- 英文论文关键词：propofol ; Hypoxia reoxygenation ; Endothelial cells ; Caspase 3 ; Bcl-2
- 会议召开时间：2016-11-25
- 会议录名称：湖南中医药大学学报2016/专集：国际数字医学会数字中医药分会成立大会暨首届数字中医药学术交流会论文集
- 语种：中文
- 分类号：R614
- 学会代码：HNZY
- 会议名称：国际数字医学会数字中医药分会成立大会暨首届数字中医药学术交流会
- 会议地点：中国广东珠海
- 主办单位：国际数字医学会、Digital Chinese Medicine
- 学会名称：湖南中医药大学期刊杂志社
- 页数：2
- 文件大小：2115k
- 原文格式：D
- 会议级别：全国
摘要
目的研究分析异丙酚对缺氧复氧损伤人血管内皮细胞caspase-3和Bcl-2蛋白表达的影响。方法建立人脐静脉内皮细胞缺氧复氧损伤模型,把细胞缺氧培养30分钟后予以复氧,或者是加入不同浓度异丙酚进行30分钟的孵育后进行缺氧复氧的处理。对复氧不同时间点用流式细胞仪对凋亡细胞数量进行计数,同时应用免疫细胞化学方法对血管内皮细胞caspase-3和Bcl-2蛋白变化进行检测。结果对照组中Bcl-2蛋白表达较低,随着复氧时间的延长Bcl-2蛋白显著下降,在6小时处于较低水平,48小时部分恢复。在25联合组中和相应的缺氧复氧组相比,Bcl-2蛋白表达间具有显著性差异(P<0.05),50、100联合组和相应的缺氧复氧组相比具有显著性差异(P<0.05),并且和25联合组相比也具有显著差异(P<0.05)。结论异丙酚可以抑制缺氧复氧导致的caspase-3活化及上调Bcl-2蛋白表达,可降低缺氧复氧损伤引起的内皮细胞的凋亡。
objective to study the effect of propofol on caspase 3 Bcl- 2 protein expression of hypoxia reoxygenation treated human vascular endothelial cells. Method human umbilical veinendothelial cell hypoxia reoxygenation injury model was established, the cells were hypoxia cultured after 30 minutes of oxygenation, or treated with different concentrations of propofol when hypoxiacultured after 30 minutes of oxygenation. Cells in different time points after oxygenation were counted with the number of apoptosis, at the same time caspase 3 and Bcl- 2 protein changes were detectedby immunohistochemical approach. Result in the control group the Bcl- 2 protein expression was lower, with prolonged duration of reoxygenation, the Bcl- 2 protein decreased significantly at lowerlevels in 6 hour and led to partially recovery at 48 hour. Compared with related hypoxia reoxygenation group, the 25 combined group showed significant difference between in Bcl- 2 protein expression(P < 0.05), the difference was significant in the 50 and 100 combined group(P < 0.05). Compared with 25 combined group, the 50 and 100 combined group also had significant difference(P < 0.05). Conclusion propofol can inhibit caspase 3 activation and enhance the Bcl- 2 protein expression caused by hypoxia reoxygenation, and attenuate hypoxia reoxygenation injury induced endothelial cellapoptosis,.
objective to study the effect of propofol on caspase 3 Bcl- 2 protein expression of hypoxia reoxygenation treated human vascular endothelial cells. Method human umbilical veinendothelial cell hypoxia reoxygenation injury model was established, the cells were hypoxia cultured after 30 minutes of oxygenation, or treated with different concentrations of propofol when hypoxiacultured after 30 minutes of oxygenation. Cells in different time points after oxygenation were counted with the number of apoptosis, at the same time caspase 3 and Bcl- 2 protein changes were detectedby immunohistochemical approach. Result in the control group the Bcl- 2 protein expression was lower, with prolonged duration of reoxygenation, the Bcl- 2 protein decreased significantly at lowerlevels in 6 hour and led to partially recovery at 48 hour. Compared with related hypoxia reoxygenation group, the 25 combined group showed significant difference between in Bcl- 2 protein expression(P < 0.05), the difference was significant in the 50 and 100 combined group(P < 0.05). Compared with 25 combined group, the 50 and 100 combined group also had significant difference(P < 0.05). Conclusion propofol can inhibit caspase 3 activation and enhance the Bcl- 2 protein expression caused by hypoxia reoxygenation, and attenuate hypoxia reoxygenation injury induced endothelial cellapoptosis,.
引文
[1]冯春生,麻海春,岳云等.异丙酚对大鼠局灶性脑缺血再灌注时NF-κB活化和Bcl-2、Caspase-3基因表达的影响[J].中华麻醉学杂志,2006,26(5):456-459.
[2]祖剑宇,刁玉刚,陈卫民等.异丙酚对缺氧复氧损伤人血管内皮细胞caspase-3和Bcl-2蛋白表达的影响[J].中国现代医学杂志,2007,17(11):1344-1348.
[3]方爱莉,刘保江.丙泊酚对大鼠急性心肌缺血再灌注损伤Cas Pase-3 Bcl-2/Bax表达的影响[J].中国药物与临床,2010,10(10):1120-1122.
[2]祖剑宇,刁玉刚,陈卫民等.异丙酚对缺氧复氧损伤人血管内皮细胞caspase-3和Bcl-2蛋白表达的影响[J].中国现代医学杂志,2007,17(11):1344-1348.
[3]方爱莉,刘保江.丙泊酚对大鼠急性心肌缺血再灌注损伤Cas Pase-3 Bcl-2/Bax表达的影响[J].中国药物与临床,2010,10(10):1120-1122.