摘要
目的:观察缺氧预处理(PC)对于自发性高血压大鼠(SHR)血管平滑肌细胞(VSMC)缺氧复氧(H/R)损伤的延迟保护作用,并探讨其可能机制。方法:对VSMC于缺氧PC24h后进行H(2h)/R(1h),结束实验时测定其H/R后细胞存活率、乳酸脱氢酶(LDH)释放和ATP含量,并测定其金属硫蛋白(MT)量。结果:缺氧PC明显减轻H/R造成的SHR的VSMC存活率下降、ATP耗竭和LDH释放,并使细胞内应激蛋白MT含量升高1.3倍,上述指标与正常血压对照组WKY大鼠VSMC的结果相近。结论:培养的SHR的VSMC亦存在PC的延迟保护作用,其保护机制涉及MT合成增多。
Objective: To investigate the delayed protective effects of hypoxic preconditioning on vascular smooth muscle cells (VSMC) of spontaneous hypertensive rats (SHR) subjected to hypoxia/reoxygenation (H/R) injury and the protective mechanism. Methods: Hypoxic PC was performed 24 h prior to H/R injury in VSMC cultured from SHR and WKY rats, and the cell viability, lactate dehydrogenase (LDH) release and cellular ATP content after H/R were determined. Metallothionein (MT) content in VSMC was also detected. Results: Hypoxic PC decreased H/R induced cellular LDH release, ATP depletion and improved cell viability, and increased MT content in VSMC of SHR. The above effects were similar to that in VSMC of WKY rats. Conclusion: Cultured VSMC of SHR have delayed protective effect of hypoxic PC. PCinduced cellular MT increase is involved in the protective mechanism.
出处
《北京医科大学学报》
CSCD
1998年第2期124-126,共3页
Journal of Peking University(Health Sciences)
基金
国家自然科学基金
关键词
高血压
血管平滑肌细胞
预处理
缺氧
Hypertension/metab Muscle, smooth, vascular/metab Oxygen/metabPreconditioning☆