摘要
目的观察地氟醚预处理对缺氧/复氧(A/R)损伤内皮细胞凋亡相关基因Bcl-2及Bax表达的影响,探讨地氟醚预处理抑制细胞凋亡的机制。方法选用人脐静脉内皮细胞株(ECV304)。将细胞分为五组,即A/R组(A组)、A/R+肿瘤坏死因子α(TNF-α)10 ng/ml组(B组)、地氟醚1.0MAC预处理+A/R组(C组)、地氟醚1.0 MAC预处理+A/R+TNF-α10 ng/ml组(D组)和空白对照组(E组)。应用Real-time PCR、Western Blot方法检测各组细胞中Bcl-2及Bax mRNA和蛋白水平。结果Real-time PCR和Western Blot结果提示,与E组相比,A、B组Bcl-2表达降低,Bax表达升高(P<0.05或P<0.01)。经地氟醚预处理后,C、D组细胞较相应未经预处理的A、B组Bcl-2表达增加,Bax表达降低(P<0.05或P<0.01)。结论地氟醚预处理可通过调节Bcl-2及Bax的表达来抑制缺氧/复氧所引起的内皮细胞凋亡。
Objective To observe the effect of desflurane preconditioning on the expression of apoptosis related genes Bcl-2 and Bax in endothelial ceils induced by Anoxia/Reoxygenation(A/R). Methods This study is based on human umbilical vein endothelial cell line (ECV304). The ECV304 ceils were divided into five groups: A/R group (A group), A/R + TNF-α 10 ng/ml group (B group), Des + A/R Group (C group), Des + A/R + TNF-α 10 ng/ml group (D group) and control group (E group). The expression of Bcl-2 and Bax in each group was detected by the methods of Real-time PCR and Western Blot. Results In both A and B groups, compared with E group, the expression of Bcl-2 was reduced, and the expression of Bax was increased (P〈0.05 or P〈0.01). However, after desflurane preconditioning, an increased expression of Bcl-2 and deceased expression of Bax was observed in C and D groups as compared to A or B group, respectively. Conclusion Desflurane preconditioning can modulate the expression of Bcl-2 and Bax to reduce endothelial cell apoptosis caused by A/R.
出处
《临床麻醉学杂志》
CAS
CSCD
2008年第7期598-600,共3页
Journal of Clinical Anesthesiology
基金
2006年度复旦大学青年科学基金项目