Study On Molecular Mechanisms Of The Protective Action Of Electroacupuncture On Ischemic Cerebral Injury

In traditional Chinese medicine, Ischemic Cerebral Vascular disease which categorized into wind stroke shows high rate of attack, death and disability, the prevention and treatment of which is an important subject on medicine and society for it's terrible harm to people's health. Acupuncture for ischemic stroke is much better than other treatments with convenience, availability, cheapness and convinced by both experts and patients of ischemic stroke all over the world. In order to study the action mechanism of acupuncture and moxibustion in treating this disease more systematically and comprehensively, the following context has several aspects. 1. Literature Research Tracing the originals, from the appearance of Yellow Emperior's Internal Medicine as the first classical works of traditional Chinese medicine to the dynasties of Tang, Shong, Yuan, Ming and Qing, the predecessors had done much to ancient medical books in the aspects of the stroke's term, etiology, pathogenesis and therapy. In the late years, many articles carefully explain much research of the disease such as clinical experiments, ischemic cerebral injury of pathological and physiological basis in modem science and acupuncture effect. All that has been done founds the theorical basis of further studying acupuncture for ischemic stroke. 2. Experiment Research The research aimed to the molecular mechanism of ischemic stroke. Using immunohistochemical and other methods, the protective actions of electroacupuncture (EA) stimulating meridian point of the DU meridian on ischemic cerebral injury were systematically studied. The results as follows: (1) Ten hours after focal brain ischemia in rats caused by occlusion of the middle cerebral artery(MCAO), TUNEL method was used to observe the effect of EA on the apoptosis of neurocyte. Result: In control group, no TUNEL dying positive cell was seen. Large members of positive cells were seen in infarct area of the pallium of the rats in ischemia group ten hours after focal brain ischemia. In ischemia and EA group, the positive cells decreased markedly. There was a significantly difference between ischemia group and ischemiam and EA group (PKO.O 1). That means EA may restrain the apoptosis of the neurocyte after focal brain ischemia. and has protective action on ischemia cerebral injury. The possible mechanism of the action were preventing lipid peroxidation in brain, restraining excit toxic action, regulating calcium steady state and preventing over loading of intracellular calcium. So the startup of apoptosis gene were preventing, anti-apoptosis gene were promoted and anti-apoptosis aim was acquired. (2) Ten hours after focal cerebral ischetnia in rats caused by MCAO, the expression of tyrosine kinase (TrkA), Nerve Growth Factor Receptor (NGFR), was detected with immunohistochemical method, and the effect of EA was observed. Results: in control group, the expression of TrkA was less. The quantity of the cells with positive expression of TrkA increased to a certain degree in ischemia group. But the extension of the expression was weak too. The expression increased remarkably in quantity and extension in ischemia and EA group than which in control group or ischemia group (P