电针对局灶性脑缺血/再灌注大鼠IL-1Ra mRNA表达的调节

目的 :观察电针 (EA)对局灶性脑缺血 /再灌注大鼠IL 1RamRNA表达的调节作用。方法 :采用线栓法制备SD大鼠局灶性大脑中动脉阻塞缺血 /再灌注 (MCAo)模型 ,并应用RT PCR的方法进行观察。结果 :MCAo大鼠缺血侧大脑皮层在再灌注后 1 2hr和 2 4hrIL 1RamRNA表达增加 ;在缺血侧纹状体缺血再灌注后 1 2hrIL 1RamRNA表达明显增加 ,但再灌注后 2 4hr表达明显降低 ,电针可使IL 1RamRNA的表达明显增加。结论 :EA可使内源性IL 1RamRNA表达增加 ,从而使IL 1Ra表达增加 ,对脑缺血起保护作用 ,这也可能是EA抗脑缺血损伤的机制之一。

Effect of EA on IL-1Ra mRNA Expression of the Brain Tissues in Cerebral Ischemia-reperfusion Rats

Objective: To investigate the protective mechanisms of electroacupuncture (EA) on cerebral ischemic injury. Methods: SD rats were randomly and evenly divided into control group, sham operation group, ischemia(I) 2 hr group, I reperfusion (R) 2 hr group, I R 6 hr group, I R 12 hr group, I R 24 hr group, I R 2 hr+EA group, I R 6 hr+EA group, I R 12 hr+EA group and I R 24 hr+EA group (with 5 rats in each group). "Baihui"(GV 20) and "Shuigou"(GV 26) of the 4 ischemia+EA groups were stimulated with EA (20/4 Hz, 3 mA and duration of 1 hr). RT PCR was used to explore the effects of electroacupuncture (EA) on interleukin 1 receptor antagonist (IL 1Ra) mRNA expression in rats with middle cerebral artery occlusion (MCAo). Results: IL 1Ra mRNA expression was rapidly induced by MCAo, and increased significantly at 12 hr (0.770±0.076), reaching a peak level at 24 hr after reperfusion in the ischemic cortex area(0.994±0.098) compared with normal group (0.475±0.069,P<0.001). IL 1Ra mRNA also increased significantly after 12 hr IR in striatum (0.796±0.103) compared with normal group (0.521±0.061,P<0.05). However, IL 1Ra mRNA decreased after 24 hr IR in ischemic striatum (0.500±0.118). The expression of IL 1Ra mRNA in EA group increased significantly compared with ischemia control group after reperfusion 12 hr (0.890±0.087 vs 0.770±0.076 ) and 24 hr in cerebral cortex (1.201±0.155 vs 0.994±0.098 ) and 24 hr in stratium (1.046±0.132 vs 0.500±0.118),P<0.05,P<0.001. Conclusion: The results indicated that EA could upregulate the IL 1Ra mRNA expression in ischemia rats, that may contribute to the protective action of EA in reducing ischemic brain injury.