The Experimental Study Of The Effects Of Shenmai Injection On The Neuronal Mitochondria-DNA Deletion And Apoptosis Related Gene Expression In Rat Brain After Intracerebral Hemorrhage

With Sprapue-Dewley rat models with intracerebral hemorrhage(ICH), This research observed the effects of Shenmai(SM) Injection on the pathologic changes of the neuronal structure in hippocampal gyrus CA1 areas, expression of Bcl-2 mRNA, Bax mRNA, C-myc mRNA, PDGF-A mRNA and mitochondria-DNA deletion in the areas around the hematoma. Results:1. The effect on the pathologic changes of neuronal structure in hippocampal gyrus CA1 areas in rat models with ICH. 7days after ICH in the rats,We examined the brain tissues of the rats and found that SM Injection had effects on antagonizing the pyramidal cells apoptosis in the hippocampal CA1 areas and alleviating the pathologic signs of the neuronal system in rat models with ICH. The results suggested that SM Injection could antagonize the neuronal apoptosis in rat models with ICH.2. The effect on the expression of Bax mRNA and Bcl-2 mRNA in the areasaround the hematoma. The levels of Bax mRNA and Bcl-2 mRNA increased significantly in rats 12 to 48 hours after ICH with a peak at 24th hours after ICH. SM Injection Could increase the levels of Bcl-2 mRNA and decrease the levels of Bax mRNA. The results suggested that SM Injection could antagonize the neuronal apoptosis by regulating the expression of Bcl-2 mRNA and Bax mRNA.3. The effect on the expression of C-myc mRNA and PDGF-A mRNA in the rats with ICH. The levels of C-myc mRNA and PDGF-A mRNA reached the peak 12hours after ICH. SM Injection had no significant effect on the expression of C-myc mRNA at initial phase, but decreased the levels of PDGF-A mRNA and prolonged the time of expression. The results suggest that SM Injection could antagonize the delayed injury of the neuronal cells by regulating the expression of PDGF.4. The effect on mitochondria-DNA(mtDNA)deletion in the rats with ICH . There was mitochondria-DNA deletion to different degrees in the cerebral tissues of the rats after ICH. SM Injection could protect mitochondria-DNA and decrease the degree of deletion in the rat brain. The results suggested that SM Injection might antagonize the delayed injury of the brain and neuronal apoptosis by protecting the mitochondria-DNA.