摘要
目的 探讨吡那地尔 (Pinacidil)预处理 (preconditioning ,PC)对失血性休克大鼠保护作用的机制。 方法 (1)大鼠 90只 ,随机分为正常组 (N组 ,10只 )、对照组 (C组 ,40只 )和预处理组(PC组 ,40只 ) ,PC组大鼠用Pinacidil进行预处理 ,2 4h后将对照组和预处理组大鼠复制成失血性休克模型 ,用Westernblot方法观察不同时相点大鼠心肌组织细胞型磷脂酶A2 (cPLA2 )的表达变化 ;(2 )大鼠 6 0只 ,随机分为对照组 (C组 ,30只 )和预处理组 (PC组 ,30只 ) ,PC组大鼠用Pinacidil进行预处理 ,然后分别在 2 4,48,72h 3个不同时间点将两组大鼠复制成失血性休克模型 ,用Westernblot方法观察PC对大鼠心肌和肝脏组织热休克蛋白 70 (hsp70 )表达的影响。 结果 (1)PC组心肌组织cPLA2 的表达较弱 ,而C组表达很强 ;(2 )C组hsp70表达很弱或检测不到 ,PC组心肌和肝脏hsp70表达很强 ,2 4h达到高峰 ,48h和 72h逐渐减弱。 结论 Pinacidil预处理可能是通过诱导hsp70过度表达和抑制PLA2 的表达保护“休克细胞” 。
Objective To investigate the mechanisms of Pinacidil preconditioning protection of hemorrhagic shock rats. Methods The rats were divided into 3 groups: a normal group (n=10), a control group (n=40) and a preconditioning group (n=40). Pinacidil preconditioning was processed 24 h before making the hemorrhagic shock model. The cPLA 2 expression in myocardium was observed at different time points with western blot; Pinacidil preconditioning was processed 24, 48 and 72 h before making the hemorrhagic shock model to observe hsp70 expression in myocardium and liver tissue with western blot. Results Pinacidil preconditioning could increase hsp70 expression and decrease cPLA 2 expression. Conclusions Pinacidil preconditioning protects 'shock cell' by inducing hsp70 overexpression and inhibiting cPLA 2 expression, which is responsible for protecting myocardial and liver tissues of the hemorrhagic shock rats.
出处
《中华创伤杂志》
CAS
CSCD
北大核心
2001年第4期232-234,共3页
Chinese Journal of Trauma