眼针与体针对脑缺血再灌注损伤24h大鼠氧自由基和细胞间黏附分子表达的差异研究

Study on Differences of Oxygen Free Radicals and ICAM-1 Expression Between Eye Acupuncture Therapy and Body Acupuncture Therapy in Rats with Acute Cerebral Ischemia-Reperfusion Injury for 24 Hours

目的:观察眼针与体针对24 h脑缺血再灌注损伤模型(CIRI)大鼠血清中SOD和MDA含量以及脑组织细胞间黏附分子-1(ICAM-1)表达的影响,以探讨眼针治疗CIRI机制与体针的差异。方法:线栓法复制大鼠急性脑缺血再灌注损伤模型,将SD大鼠48只随机分为正常对照组、24 h假手术组、24 h模型组、24 h穴区组、24 h体针组以及24 h穴区外组。脑缺血再灌注后24 h采用ZeaLonga评分法进行大鼠神经功能评分,化学比色法检测血清中SOD、MDA的含量,RQ-PCR方法和Western Blot方法测定脑组织ICAM-1 mRNA以及蛋白表达。结果:与模型组比较,穴区组大鼠神经功能缺损评分明显下降;血清中SOD活性明显升高、MDA含量明显下降;脑组织ICAM-1蛋白及mRNA表达明显下调(P<0.05)。眼针组与体针组比较无统计学差异。结论:眼针与体针均能改善大鼠24 h脑缺血再灌注损伤;其机制与血清中SOD活性升高、MDA明显下降以及脑组织ICAM-1表达下调有关,眼针与体针差异不明显。

Objective:To study the effect of the eye acupuncture therapy on cerebral oxygen free radicals and ICAM-1 expression in rats with cerebral ischemia-reperfusion injury for 24 hours and the related mechanism.Methods:We made the rat model of cerebral ischemia-reperfusion by the suture method. Forty-eight SD rats were randomly grouped into normal control group, model group, sham operation group, eye acupuncture group, body acupuncture group and point area group. After reperfusion for 24 hours, the neural function score was adopted by ZeaLonga scoring marks. The method of chemical colorimetry was used to detect the contents of SOD and MDA in serum. The methods of Western-blotting and RT-PCR were used to detect the changes of ICAM-1 protein and mRNA in rat brains.Results:Compared with the model group, the neurologic impairment score of the eye-acupuncture group get lower. We found that the SOD activity increased significantly and the content of MDA decreased evidently in serum. The expression of the ICAM-1 protein and mRNA in rat brains was significantly reduced after the eye acupuncture therapy(P<0.05). However,there was no statistical difference between the eye acupuncture group and the body acupuncture group.Conclusion:Both the methods of eye acupuncture therapy and body acupuncture therapy can reduce the cerebral ischemia-reperfusion injury by increasing the SOD activity, decreasing the content of MDA in serum and inhibiting the expression of the cerebral ICAM-1 protein.