Effect Of Xingnaojing On Apoptosis Of Hippocampal Neurons In Rats After Experimental Subarachnoid Hemorrhage

Introduction Xingnaojing injection is an injection of Chinese medicine. The research shows that XNJJ can inhibit cerebral vasospasm after SAH, improve brain ischemia and hypoxia, and significantly improve rates of coma patient awake. With the role of cerebral protection, it has been widely used in neurological emergency, crisis, critical treatment and subarachnoid hemorrhage. Many studies have shown that inhibition of apoptosis could also play a role in brain protection, so this study aims to explore the effect of Xingnaojing on neuronal apoptosis in the rat SAH model and provides a theoretical basis for clinical prevention and treatment of brain injury after SAH. It is believed that the apoptosis is inducted by variable specific physiological or pathological factors, the genes directly control the apoptosis occurrence and development. External cell factors affect the expression of these genes or products activation through the signal transduction, and thus indirectly regulate the apoptosis.There are a lot of studies on apoptosis. Different types and different growth stages of cells have different apoptosis pathways, but this difference mainly shows in the early molecular mechanisms of apoptosis induced. While as soon as apoptosis starts, different early apoptotic signals all gather to a common execution pathway, causing similar characteristic morphologic and biochemical changes. Caspase-3, an important member of the Caspase family, is the common downstream effect part of the pathway, which decomposes a series of proteins necessary for cell survival, and promotes apoptosis. Bcl-2 family, an apoptosis suppressor gene, can directly control of the mitochondrial outer membrane permeability and prevent the signal transduction.The apoptosis inhibition of Bcl-2 is achieved by combining with Bax, a important pro-apoptotic gene. Bcl-2/Bax form a balanced system. Bax overexpression accelerates apoptosis, and Bcl-2 overexpression inhibites apoptosis. The Bcl-2/Bax ratio determines apoptosis occurrence. The Cyte-c can cause the Caspase family activation under the assistance of the ATP or the dATP and induce the apoptosis. Under the stimulation of the apoptotic factors, Cyte-c release and redistribution are controlled by Bax, which participate the mitochondrial membrane changes.[Methods]SAH model was constructed by two-time fresh autologous blood injection in the cisterna magna of adult male Wistar rats.35 rats were divided into 5 groups randomly:naive, saline control, SAH, XNJJ treatment 1, and XNJJ treatment 2. Gene expressions of Caspase-3, Bax, and Bcl-2 in different groups after SAH were detected using Real-Time PCR. To further identify these changes, Western blot was adopted to investigate the protein changes of these three molecules after SAH.Results:Compared with control group, Caspase-3, Bax, and Bcl-2 increased in variable degrees in hippocampus of SAH group (P<0.05), while in XNJJ treatment groups, Caspase-3 and Bax, but not Bcl-2, decreased compared with SAH group (P<0.01).[Conclusion] The study confirmed the occurrence of apoptosis in SAH, and also confirmed that XNJJ have anti-apoptosis effect. It is concluded that XNJJ can inhibite the apoptosis of hippocampal neurons and have brain protection effect.