目的 :观察头穴针刺对缺血再灌注大鼠脑内肿瘤坏死因子α(TNF αmRNA)表达的影响

探讨针刺治疗缺血性脑损伤的可能机制。方法 :采用大鼠局灶性脑缺血再灌注模型

应用原位杂交及HE染色方法观察脑缺血再灌注时TNF αmRNA的变化及缺血脑组织病理变化

以及针刺对其影响。结果 :假手术组大鼠TNF αmRNA在皮层、纹状体呈基础水平表达

脑缺血再灌注后12hrTNF αmRNA表达增强 (P <0 .0 5)

针刺可明显抑制皮层、纹状体内TNF αmRNA的表达(P <0 .0 5)

组织学中其神经组织变性、坏死及血管炎性反应也明显减轻。结论 :针刺对缺血性脑损伤的保护作用机制可能与针刺抑制脑内TNF αmRNA的表达有关Objective: To observe the effect of acupuncture on the expression of tumor necrosis factor alpha(TNF α) in focal cerebral ischemia reperfusion rats for researching the underlying mechanism of acupuncture in reducing cerebral ischemic injury. Methods: A total of 15 SD rats were randomly and evenly divided into sham operation

acupuncture and model groups. Cerebral ischemia reperfusion model was established by occlusion of the middle cerebral artery (in accordance with Koizumi's method) for 2 hr and reperfusion for 12 hr. In situ hybridization was used to detect the expression of TNF α mRNA of the sliced brain tissues. The histologic changes of the brain tissue was also observed under microscope after staining with hematoxylin eosin (HE) method. Results: Compared with sham operation group

the average optical density values of the cerebral cortex and striate body tissues in model group and acupuncture group increased significantly (P<0.05)

suggesting over expression of TNF α mRNA after cerebral ischemia reperfusion. In comparison with model group

the optical density values of the cerebral cortex and striate body in acupuncture group decreased considerably (P< 0.05)

suggesting that acupuncture can suppress the over expression of TNF α mRNA induced by cerebral ischemia reperfusion. Under microscope

the state of neuronal degeneration (vacuolation

etc.) and necrosis

leukocyte aggregation at the vascular wall and leukocyte infilitration around the blood vessels was severer in model group and lighter in acupuncture group. Conclusion: Scalp acupuncture can downregulate cerebral ischemia reperfusion induced over expression of TNF α mRNA

which may contribute to the effect of acupuncture in protecting cerebral neurons from ischemia reperfusion injury.