摘要
目的检测远隔缺血后处理(remote ischemic post conditioning,RIPC)对脑缺血再灌注(cerebral ischemia reperfusion injury,CIR)损伤的保护作用,并观察RIPC对CIR损伤后自噬-溶酶体途径的影响。方法用线栓法制大鼠大脑中动脉闭塞(MCAO)局灶性脑缺血再灌注模型,在缺血即刻用动脉夹夹闭股动脉15min再放开15min,重复3次,进行后处理干预。TTC染色法测定脑梗死体积,HE染色观察形态学变化,免疫组织化学方法检测-微管相关蛋白质1轻链(MAP1-LC3)和组织蛋白酶B(Cathepsin B)。观察RIPC对神经缺损症状、脑梗死体积,自噬相关因子的影响。结果 RIPC干预CIR,损伤程度减轻,行为功能改善,有显著统计学差异(P<0.01)。RIPC能减少CIR后脑梗死体积(P<0.01)。HE染色显示RIPC能改善CIR病理损伤程度,脑组织神经元损伤程度明显改善。免疫组织化学染色结果显示,RIPC组较I/R组LC3、Cathepsin B表达增加,差异显著(P<0.05)。结论 RIPC减轻CIR损伤,具有神经保护作用。RIPC的脑保护作用可能与诱导自噬-溶酶体途径有关。
Objective Detecting the protective role of remote ischemic post conditioning (RIPC) against cerebral ischemia reperfusion injury (CIR) and studying the effects of remote ischemic post conditioning on the autophagy-lysosomal pathway in rats following cerebral ischemia and reperfusion. Methods The focal ischemia and reperfusion rat model was established with suture method. The remote ischemic post-conditioning was performed with bilateral occluding of bilateral femoral arteries for 15min and reperfusion for 15min, repeated for 3 times after 90 min ischemia. The neurological deficit scores were determined before killing, pathohistological changes of injured neurons were demonstrated by HE staining. The formation of autophagosome and activation of lysosome in neuron were observed after cerebral isehemia reperfusion, immuno- histochemistry was employed to determine the expression of LC3 and Cathepsin B in ischemic penumbra. Results The neurologic deficit scores in RIPC group showed significantly improved functional outcomes (P 〈 0.01 ). RIPC significantly reduced infarct volume at 24 hours (P 〈 0.01 ). HE staining showed RIPC could improve CIR degree of pathological dam- age, brain tissue neuronal damage were significantly improved. The formation of autophagosomes and enhanced presence of lysosomes were detected by LC3 and Cathepsin B immunohistochemistry. Autophagy levels in penumbral tissues were ele- vated in neurons of RIPC rats (P 〈0.05 ). Conclusion Remote ischemic post conditioning has a neuroprotective effects on the cerebral ischemia in rats. One of the mechanisms of neuroprotections by remote isehemie post conditioning may be due to the increase of autophagy.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2013年第9期772-776,共5页
Journal of Apoplexy and Nervous Diseases