| Objective:After studying the protective effect of ischemic adaptation and voluntary movement of microRNAs hippocampal changes in ischemia-reperfusion injury and traumatic brain injury hippocampus cells. Comparison of the two tissue damage in the hippocampus in microRNAs expression differences. The purpose of screening and regulation related microRNAs target protein has a protective effect through informatics research methods. Verification purposes microRNAs regulate relations between the target protein, thus confirming the protective effect of endogenous microRNAs on hippocampal tissue injury.Method:Using whole brain ischemia and reperfusion in mice independent motion model adaptation model and traumatic brain injury after. Modeling of cognitive function before and after evaluating the situation by water maze test methods. Observed by Tunel staining method in the case of apoptosis in the hippocampus; by the expression of microRNAs chip screening technique before comparing modeling within hippocampal microRNAs; the use of bioinformatics software selected for screening purposes microRNAs; purpose agonists and inhibition of microRNAs agents and related protein phosphorylation inhibitor mechanism observed in the purpose of the anti-apoptotic protein pathway microRNAs, thereby further observed changes in the regulatory mechanism between the key anti-apoptotic protein STAT3 pathway and microRNA purpose, the protection mechanism within endogenous microRNAs are confirmed.Result:On the basis of the model successfully produced on the use of water maze test methods, adapt and self-discovery after ischemic exercise on cognition have a significant protective effect; Tunel staining methods can be found in these two tissues and cells against apoptosis in the hippocampus; use mouse hippocampus microRNAs chip screening technique for this two methods of screening, found that compared with simple mouse hippocampus ischemia-reperfusion injury, ischemic change adaptation triggered expression of 9 microRNAs, including 4 expression down 5 expression increased by bioinformatics analysis showed significantly reduced ischemic adaptation miR-101 expression in the hippocampus of; within TBI mouse hippocampus independent movement, compared to TBI group alone, there are 18 of microRNAs expression changes, increased expression has nine, decreased expression has nine. By comparison bioinformatics screening and analysis of experimental data show that ischemia.After the reduction of miR-101 adaptation enhances JAK2-STAT3-BCL2 pathway in the hippocampus plays an anti-apoptotic role; after voluntary movement decreased expression of miR-34a may be involved in the pathological process of apoptosis-related hippocampal tissue, particularly involved in the IL-6-mediated IL-6R/STAT3/BCL2 antiapoptotic feedback loop, and enhanced anti-apoptotic effect of the loop.Conclusion:MicroRNAs differentially expressed in the hippocampus may be one of the endogenous protective mechanism of anti-apoptotic hippocampal tissue. miR-101 in ischemic tissue in the hippocampus of mice under conditions of reduced expression of adaptation, then increasing the JAK2 target protein expression, and promote further activation of post-ischemic adaptation JAK2/STAT3 pathway, and in the absence of ischemic postconditioning only under conditions inhibiting the expression of miR-101 alone in the hippocampus of mice is not effectively activate the JAK2/STAT3 pathway; miR-34a involved in the apoptotic process secondary injury after TBI hippocampus, independent movement of the hippocampus by down TBI intracellular expression of miR-34a and by miR-34a/IL-6R/STAT3/BCL2 feedback loop play against hippocampal neuronal apoptosis. |
