Part Of The Mechanism Of Buyanghuanwu Decoction And Its Active Fraction Against Brain Ischemia And Reperfusion Injury

With the living gerbils model of cerebral ischemia reperfusion injury, this research studied the effects of Bu Yang Huan Wu Decoction(BYHWD)and its available compostion combination on pathologic change of neuronal structure in hippocampal gyrus CA1 area, neuronal apoptosis, the expression of heat shock protein70 (HSP7O) and the reactive Astrocyte activation after cerebral ischemia and reperfusion. The results showed: 1. Effect on pathologic change of neuronal structure in hippoccampal gyrus CA1 area: After cerebral ischemia for 15 mm followed. reperfiision for Sd in cerebral tissue, BYI-IWD and its available composition combination have similar effects on increasing the neuronal density and improving the pathological changes in hippocampal CA1 area. The results suggested that BYHWD and its available composition combination could contagonize the loss of the neuron in hippocampal gyms CA1 area and the delayed injury of cerebral tissue after cerebral ischemia. 2. Effect on the expression of HSP7O: After cerebral ischemia for 15 mm lg- followed reperfusion for 48h in cerebral tissue, the level of HSP7O mRNA and protein increased significantly. Both the BYI-IWD and its available composition combination decreased the level of HSP7O mRNA remarkably, the prior is superior to the latter. Neither the BYHWD nor its available composition combination showed any effects on the expression of HSP7O protein. The results suggested that downregulating the expression level of HSP7O mRNA might result in the anti-ischemia effect of BYHWD and its available composition combination, and this is benefit for the repair of the neurons after ischemia. 3. Effect on neuronal apoptosis in hippocanipal gyrus CA1 area: After cerebral ischemia for 15 mm followed reperfusion for 48h, the percentages of neuronal apoptosis increased obviously, both BYHWD and its available composition combination could antagonize neuronal apoptosis. The results suggested that BYHWD and its available composition combination could antagonize the delayed injury of cerebral tissue maybe by antagonizing neuronal apoptosis. 4. Effect on. reactive astrocyte activation after cerebral ischemia: There were no expression of GFAP in cerebral tissue at 15 mm following cerebral ischemia, but the expression of GFAP reached peak after cerebral ischemia for 15 mm followed by reprefusion for 24h, it occurred mainly in hippocampal CA1 area. BYHWD could weaken the expression of GFAP, the effect of its available composition combination was similar to it. Expression if GFAP weakened after cerebral ischerria for 15 mm followed by reperfusion for 48h. Compared with model group, the expression of GFAP strengthened in BYHWD and its available composition combination group, comparable expression of GFAP were observed in both groups. The results suggested that Astrocyte activation occurred mainly during reperfusion after cerebral ischemia. BYHWD and its available composition combination could inhibit activation of astrocyte by antagonizing ischemic injury during early stage of reperfusion, both helped improve the repair of lesion by facilitating astrocyte activation during late stage of reperfusion~...