The Experimental Of NXKKFY On Oxygen Free Radical And NO,NOS In Rats Of Cerebral Ischemia-reperfusion Injury

Cerebrovacular disease (CVD) is a common and frequently encountered disease of nervous system. The death rate of CVD is about 10% of all the disease. There are 50%-70% survivor of CVD who remain paralysis aphasia and other severe disabilities. Ischemic stroke also called cerebral infarction (CI), which is a common type of CVD, because of ischemia or hypoxia, induce ischemic necrosis or cerebromalacia of brain tissue. CI is a serious harmful disease of mankind. Anastate the blood perfuse is the most common treatment of CI. But if the time of cerebral blood flow recanalization beyond the time window, the brain injured can become aggravate. It is called reperfusion injury. For this condition, the studies on the product mechanism and the treatment of reperfusion injury are more important than before. At the same time, reperfusion injury become a hot spot of study and research. NXKKFY is developed from the tradition famous prescription of BYHWT. It is a utility prescription of treatment on ischemic stroke which belong to blood stagnancy due to deficiency of QI in our department (The department of traditional Chinese medicine in JI LIN university). In clinical, it can be authenticated that NXKKFY could improve cerebral ischemia condition obviously and soften clinical symptom. At the same time, we find NXKKFY can decrease reperfusion injury. We built animal model and observe the effect of cerebral ischemia-reperfusion injury in rats after treated by NXKKFY. We approach the mechanism of NXKKFY and want to have reliable reason for develop and utilize it. Rats were randomly divided into normal control group, pretend operation group, negative control group, nimotop group, low-dose group of NXKKFY, midst-dose group of NXKKFY and high dose group of NXKKFY. Rats were general anesthesia by 10% formalin, were clipped bilateralis arteria carotis communis by no damaged bulldog clamp to cause cerebral ischemia. It is the model of cerebral ischemia. After 2 hours, we relax the bulldog clamp and recanaliza the arteria carotis communis for 24 hours. It is the model of reperfusion injury. The rats were treated by NXKKFY or nimotop. Intragastric administration for 10 days, rats were killed to observe and analyze the effect of MDA, SOD, NO and NOS in blood serum and brain homogenate. Pathological sections were dyed to observe the histopathological changes. At the same time, we carry out the anti-hypoxia test of mice in condition of normal pressure: Mice were randomly divided into normal saline control group, nimotop group, low-dose group of NXKKFY, midst-dose group of NXKKFY and high dose group of NXKKFY. Intragastric administration for 7 days , the mice were put to the wide mouthed bottle filled with natrica calx. We test the survival time of mice from close the bottle to respirationceases. Moreover, we carry out the test of cutting head. The divided and the medication is same to the anti-hypoxia test of mice in condition of normal pressure. Intragastric administration for 7 days, rats were cut heads quickly and recorded the persistence time of gasp. From these experiments, the following conclusions can be gain: 1. The changes of MDA and SOD: Compared with normal controlled group, the level of SOD and MDA in brain homogenate and blood serum changed very insignificant. While the level of MDA increased significantly and the level of SOD decreased significantly in negative control group; It is proved that the excessive increase of free radical and lipid peroxidation are the important pathogenesy of cerebral ischemia-reperfusion injury. The low-dose, midst-dose and high dose group of NXKKFY all can increase the level of SOD and decrease the level of MDA at the same time, which are very significant difference by compared with negative control group .The high dose group of NXKKFY have better capability to increase the level of SOD and decrease the level of MDA than other dose group of NXKKFY, but have no significant differences of statistics. All dose group of NXKKFY have no significant differences of statistics by compared with nimotop group. All that proved the low-dose group of NXKKFY, midst-dose group of NXKKFY and high dose group of NXKKFY all can increase the level of SOD and decrease the level of MDA at the same time. NXKKFY can increase the ability ofanti-oxidation and restrain the formation of lipid peroxidation . So NXKKFY can play a good role in decrease the injury of ischemia-reperfusion. 2. The changes of NO and NOS: Compared with normal controlled group, the level of NO and NOS in brain homogenate and blood serum changed very insignificant. While the level of NO and NOS increased significantly in negative control group; It is proved that the excessive increase of NO and NOS are the important pathogenesy of cerebral ischemia-reperfusion injury. The low-dose, midst-dose and high dose group of NXKKFY all can decrease the level of NO and NOS, which are very significant difference by compared with negative control group .The high dose group of NXKKFY have better capability to decrease the level of NO and NOS than other dose group of NXKKFY, but have no significant differences of statistics. The midst-dose group of NXKKFY and high dose group of NXKKFY no significant differences of statistics by compared with nimotop group. All that proved NXKKFY can decrease the level of NO and NOS. NXKKFY can increase the ability of restraining the formation of NO and NOS. So NXKKFY can play a good role in protecting the brain tissue. 3. Pathological change: As pathology result show, after cerebral ischemia-reperfusion, the rats　brain tissue cells of negative control group arranged chaotic, cell population decreased. The degenerationof tissue cells became generally. The bulk of tissue cell became increased. The dyeing of tissue cell became light and the endochylema of tissue cell became rarefactful at the same time. All that show the pallium appeared the change of cerebral ischemia-reperfusion injury. Compared with negative control group, the tissue cells of the low-dose, midst-dose and high dose group of NXKKFY became regularity and increased. The hydrops of cells became decreased. The degenerating cells became little than before at the same time. All that proved the degree of injury of neurocytes is lighter than negative control group .It can prove that NXKKFY can decrease the cerebral ischemia-reperfusion injury of rats. 4. The anti-hypoxia test of mice: Compared with normal saline group, the mice of midst-dose and high dose group of NXKKFY can have a longer survival time which proved NXKKFY can increase the capability of anti-hypoxia in mice. NXKKFY can decrease the brain injury by increase the anti-hypoxia capability of neurocytes. 5. The cut head test of mice: Compared with normal saline group, the mice of midst-dose and high dose group of NXKKFY can have a longer gape breath time, which proved NXKKFY can increase the capability of anti-hypoxia in mice. NXKKFY can decrease the brain injury by increase the anti-hypoxia capability of neurocytes. As a result, we consider that NXKKFY can increase the level of SOD and decrease the level of MDA. At the same time, NXKKFY...