The Protective Effects Of Panax Notoginsenoside Saponins On Neuron Ceil Induced By Ischemia-repefrusion

Background: Brain astrocytes (astrocyte,AS) is the central nervous system (CNS)intrinsic number absolute advantage in a large glial cells,was seen in neurons of the wholedevelopment process plays an important role in. a series of central nervous system diseases,such as stroke. The purpose of this study is to explore the cultured primary astrocyteoxygen-glucose deprivation(OGD) in vitro model,to investigate the protective effects ofpanax notoginsenoside saponins and its action mechanism in cell ischemia-reperfusionmodel.Ischemia is characterized by reduced blood flow to the cerebral circulation cerebralvascular diseases.Astrocytes (astrocyte,AS) is the central nervous system (CNS) intrinsicnumber absolute advantage in a large glial cells, thought to play an important role in thedevelopment of the whole process of neurons,astrocytes and neurons more tolerance thanischemic injury, in the nervous system disease plays a dual role of injury and protection.Therefore, in vitro and in vivo conditions of ischemia and hypoxia, the reaction can providekey based on the treatment of cerebral ischemia. Panax Notoginsenoside saponins(PNS) isthe active ingredient of total saponins purified from traditional rare medicinal herbs.Pharmacological studies suggest, can increase cerebral blood flow, improve microcirculation;inhibition of platelet aggregation, reduce blood viscosity, can block the calcium channel, theinhibition of intracellular calcium overload. In this paper, we study Panax Notoginsenosidesaponins in astrocytes induced by ischemic injury of the role and its mechanism.Objective: To investigate PNS neuroprotective effects on oxygen free radicals removaland lipid peroxidati, mitochondria membrane and apoptosis by assay Bax、Caspase-3andBcl-2、antioxidant enzyme SOD (superoxide dismutase), GSH-PX (glutathione peroxidase)and lipid peroxide (malondialdehyde) of MDA content by through cultured astrocytes cellsafter ischemia-reperfusion injury.Methods: An in viro model of glucose oxygen deprivation and subsequentreoxygenation was developed in attempt to determine the mechanisms underlying I／Rinjury.Cultured astrocyte cells were designed in three groups：normal group，ischemia group(OGD3h, reoxygenation18h), PNS group(total saponins in intervention group were given 10,20,40,80μg/ml),detection of cell culture supernatants of SOD, GSH-PX, MDA andBax and Bcl-2, Caspase-3. The mitochondrial membrane potential were stained byRhodamine123by flow cytometric detection of mitochondrial membrane potential.Result：Cultured astrocytes in hypoxia reoxygenation injury, The superoxide dismutase(SOD) activity and glutathione peroxidase (GSH-PX) activity decreased, MDA increasedmalondialdehyde content. The results proved that PNS increased intracellular SOD andGSH-PX activity, decreased MDA content. After Hypoxia and reoxygenation injury,apoptosis related protein Bcl-2protein expression decreased, expression of Bax andCaspase-3protein increased. PNS could increase expression of Bcl-2protein and preventischemic astrocytes mitochondrial membrane potential, inhibit the expression of Bax andCaspase-3protein.Conclusion: PNS could increase the expression of Bcl-2protein and effectively preventischemia-induced mitochondrial membrane potential of astrocytes, decrease the expression ofBax and Caspase-3protein. All these suggested that PNS may be a protective mechanism toimprove the activity of antioxidant enzymes, decrease the content of free radicals, andthrough the inhibition of cell apoptosis mediated by mitochondria pathway, by adjusting themitochondrial membrane of Bcl-2and Bax protein expression and mitochondrial membranepotential of astrocytes, to protect the ischemic cell injury induced.