Experimental Study Of Protective Effect Of NaoXinKang On Cerebral Ischemia Reperfusion Injury In Rat

At present a new doctrine was provided to resolve the mechanism of ischemia-induced brain damage pathology and physiology,that is cascade of damage.It include excitatory toxicity,periinfarct depolar-ization ,inflammation and prigrammed cell death .Between them,they are caused and effected each other ,and they are influenced each other.when the brain was short of blood and oxygen ,the Glu was adequately produced and stimulates the receiver because of shortage of power. Ca2+ was overload and produced a lot of ferments to reduced the cascade response. Ischemia-reperfusion injury can reduce continue strengthen response of free radical formation. Which can hit mem-brane protein, netacid and PUFA of bioligical membrane and reduce cell injury.It was reported that the GSH-PX and CAT is the best thing to clear free radical foemation. This article proved the NXKKFY have the neurol protection role in the cerebral ischemia, through examine the respect of syndromes ,Water content and Na⁺ -K⁺ -ATP ferment ,Ca²⁺-ATP ferment ,GSH-PX and CAT,and change of Histopathological observation observe the the histopathologic. NXKKFY is developed from the tradition famous prescription of Buyanghuanwu Decoction from Wangqingren.Cerebrovasular disease is a common and frequently encountered disease of nervous system. The modern medicine suffers its shortage of medications with definite curative effects and light side effects . In recent years, the The shock patients increasingly accept the treatment by Chinese traditional medications, due to their advantages such as flexibility in components, light side effects and toxicity, and suitability to long-term administration.Our department has been active in the clinical treatment, and fundamental and theoretical investigation of Zhong Feng since 1996. We independently designed and developed MXKKFY, which is mainly utilized to cure the period of emergency and lingering effects of The shock. Thousands of The shock patients were cured with the shock, which indicates MXKKFY's remarkable efficiency in clinical cases. The shock can improve definitely and markedly the clinical symptoms and signs of the The shock patients.We observed the different doses of NXKKFY that protect functions of Water content,free radical formation and fat over oxidizing after damage of cerebral ischemia-reperfusion.This experiment further investigated the pathogenesis of cerebral ischemia-reperfusian and the mechanism how MXKKFY cures it. We random assort the rats into groups, they were normal control group, false operating group ,model group ,Nimodipin group, NXKKFY large doses,middle doses and small dosage group. Focal ischemia was induced by 2 hour of closely bilateral common carotid arteries to make the model of incomplete cerebral ischemic and reper-fusion injury and followed by 24 hour reperfusion.False operating group only operate the double CAA without reperfusion. Then examining the the respect of syndromes,Water content and Na+-K+-ATP ferment ,Ca2+-ATP ferment ,GSH-PX and CAT,and changeof Histopathological observation ebserve the the histopathologic. The pathologic of brain were also been observed that every treated groups of NXKKFY all have the use of improving nerve function,and large doses group of NXKKFY and MNDP group have the bviouse use。Results:Through evaluate the rat's motive functing grades of model group.The result was the group of NXKKFY large doses rats and Nimodipin rats motive function was better than the group model (P<0.01).We found that the cerebral tissue contents of water in the group of NXKKFY large doses rats and Nimodipin rats were less than group of model (P<0.01), by examining cerebral tissue biology medical index we found that compared with false operation groups the content of GSH-PX and CATof model groups were higher (P<0.01). There are a lot of hypothesis about the mechanism of ischemia-induced brain damage, for example they are free radical formation toxin hypothesis, excitatory toxin hypothesis, hypothesis relate the pathological transformation as Ca2+ overload in the neural cell, prodrammed cell death hypothesis. At present a new pathological and biological mechanism which is cascade of damage is provided. It majorly includes excitotoxicity periinfarct depolarization, inflammation and programmed cell death. They are different dot of time. They are overlapped and relation each other. We use NXKKFY to clear free radical formation and release brain edema. Finally it can prevent cascade of damage. Perform the function of pretectal nerve.Ischemia-reperfusion injury can reduce continue strengthenresponse of free radical formation. Which can hit membrane protein, netacid and PUFA of bioligical membrane and reduce cell injury. In addition because of the increase of excitatory amino acid, and produce lots of free radical formation,finally produce MDA to damage the cell function. This article proved that the MXKKFY is the best nerve protection agent through examing the Na+-K+-ATP ferment ,Ca2+-ATP ferment in the brain tissue. NXKKFY can release the injury of ischemia of fat over oxidizing.GSH-PX and CAT are two very important therapying the ischemia-induced brain damage that can clear'O2 ,O2-and -OH.SOD and CAT can clear free radical formation and can release the injury of ischemia of fat over oxidizing.We found that GSH-PX and CAT are reduced during cerebralischemia,and AFTER the rises taked the MXKKY they are rising. MXKKFY can clear free radical formation and can release the injury of ischemia of fat over oxidizing. NXKKFY often use to cure the period of acute and lingering effects of The shock. Modern pharmacologic investigation display that many medices in this prescription have the protected function of cerebral ischemia-reperfusian.It mainly can improve micro circulation and hippocampus damage ,reduce neurosis of poison of excitatory amino acid,clear free radical ,protect calcium overload, delute blood and influce the express of genes and apoptosis so on. Above all , it can make conclusings:NXKKFY improve the motive function of the cerebral ischemia-reperfusion injury. It can...