线粒体钙单向转运体在远距预处理脑保护中的作用及其机制

Role of mitochondrial calcium transporters in the remote preconditioning on cerebral ischemia reperfusion injury and its mechanism

目的探讨肢体缺血预处理(LIP)对脑缺血/再灌注(I/R)损伤保护作用中线粒体钙单向转运体(MCU)的作用及其作用机制。方法将50只I/R损伤模型大鼠随机分为五组。模型组不干预,钌红组、精胺组、LIP组及LIP+精胺组分别于再灌注前予钌红、精胺、LIP及LIP+精胺干预。再灌注24 h观察各组神经功能评分,血清丙二醛(MDA)、乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)水平及脑皮质区Bcl-2阳性细胞数。结果钌红组及LIP组神经功能评分及血清MDA、LDH水平明显低于另三组,SOD水平及Bcl-2细胞明显高于另三组,P均<0.05。结论 CIP对I/R的脑保护作用可能与MCU有关;增强MCU活动可抑制LIP的脑保护作用。

Objective To investigate the effect of limb ischemic preconditioning（LIP） on the mitochondrial calcium uniporter（MCU） in the remote preconditioning on cerebral ischemia/reperfusion（I/R） and its mechanism.Methods Fifty I/R model rats were randomly divided into five groups,the cerebral ischemia group was not treated,the ruthenium red group,spermine group,LIP group,LIP ＋spermine group were treated with ruthenium red,spermine,LIP,LIP ＋spermine before reperfusion.After 24 h of reperfusion,neurological score,content of malondialdehyde（MDA）,activities of lactate dehydrogenase（LDH） and superoxide dismutase（SOD） content in serum,the changes of positive cells in cortex,which contains Bcl-2 protein by immunohistochemistry were observed respectively.Results Compared with the other three group,significantly lower serum MDA,LDH,significantly higher SOD,and the significantly increased expression of Bcl-2 cells were found in ruthenium red group and LIP group,all P0.05.Conclusions MCU may be one of the mechanism that LIP protect rat brain from ischemia-reperfusion;improving the activity of MCU can inhibit the cerebral protection effects of LIP.