Study On The Mechanism Of MiRNA-124/STAT3 Signaling Pathway In Reducing Neuronal Apoptosis After Intracerebral Hemorrhage In Rats

Objective:The rat model of intracerebral hemorrhage was established by injecting the rat tail artery blood into the putamen of rats,the rats were injected with miR-124 agomir and miR-124 antagomir On the basis of the model of intracerebral hemorrhage.Then measure the dynamic expression of miR-124 and STAT3 and the apoptosis and inflammatory reaction in each group.To investigate the regulatory role of miR-124/STAT3 signaling pathway in apoptosis after intracerebral hemorrhage and its related mechanisms.Methods:The 60 SPF male rats were randomly divided into 4 groups,each group consisted of 15 rats.The rats were divided into the group of cerebral hemorrhage group,miR-124 agomir group,miR-124 antagomir group and sham group.The rat model of intracerebral hemorrhage was established by injecting the tail artery of the rat to the putamen.Using Longa Zea score to determine whether the model can enter the test.Using rat brain stereo positioning instrument miR-124agomir and miR-124antagomir point injection to rat skull nucleus to regulate the expression of Mir-124.The expression of miR-124 was measured by RT-PCR,and the expression of STAT3 protein was determined by Western blot.HE staining method was used to determine the expression of inflammatory cells in the brain tissue after intracerebral hemorrhage,and Tunel staining was used to determine the neuronal apoptosis after intracerebral hemorrhage.Results:1.In the rat model of intracerebral hemorrhage,the expression of miR-124 was increased.The expression of miR-124 in the cerebral hemorrhage group and miR-124 agomir group was increased than that of the sham group significantly,the expression of miR-124 in the miR-124 antagomir group was decreased than that of the sham group,and the difference was statistically significant(p<0.05).2.The expression of miR-124 In the miR-124 agomir group was increased than the cerebral hemorrhage group,and the expression of miR-124 in the miR-124 antagomir group was decreased than that of the cerebral hemorrhage group,and the difference was statistical significance(p<0.05).3.Mir-124 can affect the expression of STAT3,the Mir-124 level of miR-124 agomir group was significantly higher than that of the cerebral hemorrhage group,but the expression of STAT3 was decreased.and the miR-124 level of miR-124 antagomir group was significantly lower than that of the cerebral hemorrhage group,but the expression of STAT3 was increased.The difference was statistical significance(p<0.05).This suggests that STAT3 may be regulated by miR-124,and the STAT3 may be the target gene of miR-124.4.The expression of STAT3 in cerebral hemorrhage model is reduced,and its decrease can promote the inflammatory reaction and apoptosis of brain cells after intracerebral hemorrhage.And miR-124 can affect the expression of STAT3,This suggests that miR-124 can regulate the inflammatory response and apoptosis of brain cells in intracerebral hemorrhage.The increase of miR-124 can induce apoptosis by inhibiting the expression of STAT3.In contrast,the decrease of miR-124 can promote the expression of STAT3 and decrease the apoptosis of cells,which may play a neuroprotective role.Conclusions:1.In the model of intracerebral hemorrhage in rats,the expression of miR-124 was increased,and the expression of STAT3 was decreased.2.In the model of intracerebral hemorrhage in rats,the expression of miR-124 could be regulated by stereotaxic injection of miR-124 agomir and antagomir.3.In the rat model of intracerebral hemorrhage,miR-124 can affect the expression of STAT3,STAT3 may be the target gene of miR-124,which is negatively regulated by miR-124.4.In the rat model of cerebral hemorrhage,miR-124 can regulate the process of apoptosis by regulating the expression of STAT3 after cerebral hemorrhage,the overexpression of miR-124 can increase nerve damage by inhibiting the expression of STAT3 and the low expression of miR-124 can reduce apoptosis by promoting the expression of STAT3 and plays a neuroprotectivet role.