益肾调督针法对脑缺血再灌注大鼠ICAM—1mRNA和蛋白表达的影响

目的：通过观察针刺对大鼠局灶性脑缺血再灌注损伤后脑组织中细胞间黏附分子-1（intercellular adhesion molecule-1，ICAM-1）mRNA和蛋白表达的影响，探讨益肾调督针法抗脑缺血再灌注炎性损伤的机制。方法：将wistar大鼠随机分为正常组、假手术组、模型组、益肾调督针法组及普通针法组，各组随机分成12、24、48h三个时间段，每个时段10例，采用栓线法制备局灶性脑缺血动物模型，运用原位杂交和免疫组织化学技术检测各组大鼠大脑缺血侧皮层ICAM-1 mRNA及蛋白表达的变化。结果：普通针法组和益肾调督针法组相应时间点ICAM—1 mRNA和蛋白表达的趋势和模型组相似，但在各时间点阳性表达均较模型组降低，且有显著差异（P〈0．05或P〈0．01）。益肾调督针法组与普通针法组相应时间点相比，有显著性差异（P〈0．05或P〈0．01），益肾调督针法组下降程度高于普通针法组。结论：益。肾调督针法可能通过下调脑缺血区ICAM-1 mRNA和蛋白表达从而防治脑缺血再灌注炎性损伤。

Effect of kidney-reinforcing and Du Meridian-regulating acupuncture on the expression of intercellular adhesion molecule-1 mRNA and protein of cerebral ischemic region in rats

Objective To study.the mechanisms of early treatment of cerebral ischemia- reperfusion（I/R） by kidney-reinforcing and Du meridian-regulating（KRDR） acupuncture method in resisting inflammation injury in rats through the observation on the efficacy of acupuncture method on the expression of intercellular adhesion molecule-1 （ICAM-1） mRNA and protein of cerebral ischemic region in rats. Methods Experimental rats were randomly allocated to antitheses group, pseudo-surgery group, model group, KRDR acupuncture group and conventional acupuncture group, to be randomly allocated to 12 24 48 hours,10 rates in each group. Cerebral I/R Model was prepared. The expression of ICAM-1 mRNA and protein was measured in groups by respectively using in-situ hybridization and immuno-histochemistry techniques. Results The direction of conventional acupuncture group and KRDR acupuncture group were similar in corresponding hours that positive group, which made the obvious significant difference expressions on corresponding hours was lower than model （P〈0.01 or P〈0.05）. The positive expressions in KRDR acupuncture group was much lower than conventional acupuncture group on corresponding hours, which made the obvious significant difference between these two groups （P〈0.01 or P〈0.05）. Conclusion Kidney-reinforcing and Du Meridian-regulating acupuncture may play a role in treatment and prevention on inflammation in cerebral ischemia/ reperfusion by down regulating the expression of ICAM-1 mRNA and protein in cerebral ischemic region.