电针对局灶性脑缺血大鼠细胞间黏附分子-1表达禾白细胞浸润的影响

目的：探讨针刺抗脑缺血再灌注炎性损伤的机制。方法：采用线栓法制作大鼠大脑中动脉缺血模型（MCAO），TIC染色，免疫组化技术及原位杂交方法检测细胞间黏附分子-1（ICAM—1）mRNA和蛋白的时程变化规律及电针的调节作用，以及检测再灌注后白细胞髓过氧化物酶（myeloperoxidase，MPO）的变化。结果：再灌注3h模型组和非穴组MPO活性均增加，24—48h达到峰值，而电针组相应MPO活性明显降低（P〈0.05）。ICAM-1mRNA和蛋白表达均发生于脑缺血，再灌注后3h，分别于再灌注12h和24h达到高峰（组内比较P〈0.01），针刺可显著降低缺血区ICAM-1mR-NA和蛋白表达（与模型组比较P〈0．01）。结论：早期针刺治疗可能通过下调脑缺血区黏附分子ICAM-1的表达．从而抑制黏附分子介导的内皮细胞与中性白细胞的黏附浸润．而防治脑缺血再灌注炎性损伤。

Effects of galvano-acupuncture on neutrophil infiltration and the expression of ICAM-1 mRNA and protein of cerebral ischemic region in rats

Objective:To study mechanisms of early treatment of cerebral ischemia-reperfusion(I/R) by acupuncture in resisting inflammation injury in rats.Method:Cerebral I/R Model was established by occlusion of the middle cerebral artery for 1h and then removal of the occlusion at 3h,12h,24h and 48h respectively.The expression of ICAM-1 mRNA and protein was displayed by using imunohistochemical ABC and in situ hybridization techniques in ischemic cerebral cortex and corpus striatum in rats.The change of leukocytes myeloperoxidase in cerebral ischemic region,was assayed with a spectrometer system.Result:The mRNA expression of ICAM-1 was detected at capillary endothelia cells in ischemic cerebral cortex at 1h ischemia-3h reperfusion and peaked at 1h ischemia-12h reperfusion,The protein expression of ICAM-1 was detected at capillary walls in post ichemia cerebral cortex at 1h ischemia-3h reperfusion and peaked at 1h ischemia-24h reperfusion and increased continually during 48h reperfusion.Both mRNA and protein expression of ICAM-1 in ischemic cerebral cortex were down-regulated considerably by galvano-acupuncture treatment(P<0.01).Conclusion:The protective effect of acupuncture on cerebral neurons under acute infarction is possible through it downregulative action on the mRNA and protein expression of ICAM-1,which caused neutrophil infiltration that induced by adhesive molecules between endothelium cell and neutrophil.