摘要
目的探讨异丙酚对缺氧复氧损伤所致人血管内皮细胞凋亡及caspase-3、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。将细胞缺氧培养30min再复氧,或加入不同浓度异丙酚孵育30min后再进行缺氧复氧处理,在复氧不同时相点(2、6、24和48h)以流式细胞仪计数凋亡细胞数量,并采用免疫细胞化学方法检测caspase-3和Bcl-2蛋白表达的变化。结果缺氧复氧后内皮细胞呈现典型的凋亡形态,复氧2h凋亡细胞数量开始增加,复氧6h时升高显著,至24h达峰值;异丙酚明显抑制复氧后细胞凋亡的发生。正常体外培养人血管内皮细胞Bcl-2蛋白表达较低,随复氧时间延长Bcl-2表达明显下调;25μmol/L异丙酚预处理可使复氧后内皮细胞Bcl-2表达升高,与相应缺氧复氧组比较差异有显著性(P<0.01),50、100μmol/L异丙酚组作用相似,不同浓度异丙酚作用呈现一定的剂量效应关系。缺氧复氧损伤使caspase-3蛋白表达增强,复氧24h后达高峰;异丙酚预处理以剂量依赖方式显著下调caspase-3表达(P<0.01)。结论异丙酚降低缺氧复氧损伤所致的内皮细胞凋亡,可能与其抑制缺氧复氧引起的caspase-3活化、上调Bcl-2蛋白表达有关。
[Objective] To investigate the effects of propofol on apoptosis and the expression of caspase-3, Bcl-2 in human vascular endothelial cells induced by hypoxia-reoxygenation injury. [Methods] The endothelial cells were cultured in normal condition for 30 min or containing propofol of different concentration and then followed by hypoxia-reoxygenation incubation. The numbers of apoptosis and the expression of caspase-3, Bcl-2 were observed. [Results] （1）The ceils showed the classical apoptotic characters after hypoxia-reoxygenation treatment. The numbers of apoptosis increased after 2 h reoxygenation and reached the peak after 24 h. Propofol inhibited the apoptosis significantly. （2）The expression of Bcl-2 in normal cells were at a lower level and was significantly down-regulated after reoxygenation, which reached the lowest at 24 h. 25 μmol/L propofol could significantly increase the expression of Bcl-2 （P 〈0.01）. 50 μmol/L propofol showed the similar results and higher concentration （P 〈0.01） and presented in a dosedependent manner. （3）The expression of caspase-3 was up-regulated and reached the peak at 24 h induced by hypoxia-reoxygenation injury. Propofol inhibited the expression of caspase-3 significantly （P 〈0.01）. [Conclusion] Propofol inhibit the apoptosis of endothelial ceils induced by hypoxiareoxygenation injury and the mechamism is possibly related to the downregulation of caspase-3 and up-regulation of Bcl-2.
出处
《中国现代医学杂志》
CAS
CSCD
北大核心
2007年第11期1344-1348,共5页
China Journal of Modern Medicine
