摘要
目的研究三氧化二砷(As2O3)预处理抗心肌缺血再灌注损伤中热休克蛋白(HSP)27的作用及调控机制。方法将16只缺血再灌注心肌损伤大鼠随机分为观察组和对照组各8只,观察组再灌注前24 h腹腔注射As2O3预处理,对照组灌注生理盐水。观察两组再灌注后心功能指标、心肌超微结构及心肌组织HSP27表达变化。结果观察组左心室舒张末期压力(LVEDP)、左心室压力收缩速率(LV+dP/dtmax)、左心室压力舒张速率(LV-dP/dtmax)较对照组明显增高,超微结构损伤亦减轻,HSP27表达量明显增加(P均<0.01)。结论 As2O3预处理对缺血再灌注心肌损伤有保护作用;其机制可能为上调HSP27表达。
Objective To investigate the mechanism of the inhibiting effect of As2O3 preconditioning on heat shock protein (HSP)27 during ischemia/reperfusion injury (IRI) in isolated rat hearts. Methods Sixteen rats with IRI were divided into observed group and control group with 8 in each, the observed group was given As2O3 preconditioning by intraperitoneal injection, and the control group was given normal saline. The ventricular function, infarct size, uhrastructure changes and the expression of HSP27 were measured. Results Compared with control group, the LVEDP, LV + dP/dtmax and LV-dP/dtmax improved significantly, the uhrastructure injury lightened, while the expression of HSP27 increased obviously (all P 〈 0.01 ). Conclusion As2O3 preconditioning can protect hearts with ischemia-reperfusion injury, the mechanism maybe related to increase the expression of HSP27.
出处
《山东医药》
CAS
2012年第15期39-41,共3页
Shandong Medical Journal
基金
温州市科技局科研基金资助项目(y20070085)