| Cerebrovascular disease is a common disease and frequently occurring that severely threatens human health and longevity. Recently, cerebrovascular disease is one of the three main causes for adult death. Intracerebral hemorrhage (ICH) is a devastating clinical condition,the incidence of mobidity and mortality from ICH remains high.Currently, there is no medical therapy available for these patientsexcept neurosurgical evacuation of the hematoma. Patients who survive ICH are usually severely disabled. The mechanisms of braininjury after ICH are not fully understood. The study of ICH in the rat attracted increasing attention.Naoxinkang for injection is a compound preparation, including:renshen,huangqi,lingzhi,shuizhi .Domestic research materials showed that Naoxinkang for injection had the effect of lowering blood pressure and stimulating antihypoxia, sheeting blood vessels, lowering cholesterol, inhibiting fat deposition on arteries, myocardium and liver. It also inhibited atherosclerotic occurrence and development. It had positive effects on brain ischemia. It hadbeen proven that Naoxinkang for injection had anti-ischemic effects on the brain as well as anti-thrombotic effects. It had also been proven that indexes of blood flow,lowering the blood platelets assembling rate.Little materials has been published about the effects of Naoxinkang for injection on intracerebral hemorrhage,in our study,to investigate the protective effects of Naoxinkang for injection on intracerebral hemorrhage in rats. The model of experimental intracerebral hemorrhage was induced in rats through infusion of 50 ul of fresh autologous blood drawn from caudal artery into the caudate uncleus . The changes in brain edema and behavior were observed. Histopathological change of rat brain subjected, Plasma SOD , MDA and NO, as well as brain tissue SOD, MDA and NO levels, were determined.We made intracerebral hemorrhage model in rats to study the effects of Naoxinkang for injection on neurocyte morphology changes and neurological scale. As the result of that the changes of neurocytes morphology are those,neurons were serious edema,neural cells looked degenerated and necrosis after intracerebralhemorrhage. Naoxinkang for injection (600mg/kg,300mg/kg,150mg/kg) reduced cellular edema, maintained the neurocyte morphology. After intracerebral hemorrhage , model rats have distinct action deficits. Some rats flexed and adducted the left limbs,some rats rotated to the left side when it crawled,some rats were unconscious and could not crawl. Naoxinkang for injection (600mg/kg,300mg/kg,150mg/kg)can reduced neurological scores(P<0.001,P<0.001,P<0.05), behavior deficits were dereased by Naoxinkang for injection. After intracerebral hemorrhage,water content of the brain and coefficient of brain in the brain regions increased sharply(P<0.05),on the 3d attained the peak when compared with the Sham-operation group, which indicates the formation of brain edema. Naoxinkang for injection (600mg/kg,300mg/kg)significantly reduced brain water content(P<0.001,P<0.05)and coefficient of brain (P<0. 01,P<0.05)decreased brain edema.NO and MDA generation , decrease SOD activity After intracerebral hemorrhage. Naoxinkang for injection (600mg/kg,300mg/kg,150mg/kg)significantly increased SOD content in plasma(P<0.001,P<0.001, P<0.05)and brain tissue(P<0.01,P<0.05,P<0.05), decreased MDA content in plasma(P<0.001, P<0.05)and brain tissue(P<0.001,P<0.01, P<0.05), as well as in plasma(P<0.001,P<0.05)and brain tissue(P<0.001,P<0.001,P<0.05)NO levels.The present study demonstrated that Naoxinkang for injection lessen the brain damage induced by intracerebral hemorrhage, which relate to the followings : Naoxinkang for injection can improve SOD activity,reduce MDA content,can maintain membrane structure. Naoxinkang for injection can inhibit NO production and lessen the brain damage. Naoxinkang for injection significantly reduced brain water content,decreased brain edema. The results suggest that Naoxinkang for injection is a potent drug,it might attenuate the neuron injury induced by intracerebral hemorrhage via antioxidant property.
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