Effect Of Dexmedetomidine On Apoptosis Of Traumatic Brain Injury Cells Via MiR-219a-5p/CACUL1 Pathway

Objective : Dexmedetomidine(Dex)was studied in microRNA-129a-5p(miR-219a-5p)/CACUL1 pathway on apoptosis of traumatic brain injury cells,which provides a theoretical basis for clinical drug research and new therapeutic strategies for TBI.Methods : Forty 8-week-old male SD rats with body weight of 220-250 g were selected and randomly divided into four groups(n=10):(1)Sham group: the head of the rats was only window-opened without blow.(2)TBI group: TBI model was established.(3)Dex group: TBI model was established + intraperitoneal injection of Dex.(4)Dex+ miR-219a-5p inhibitor(antagomir)group: TBI model was established + intraperitoneal injection of Dex+ lateral ventricle transfection of miR-219a-5p antagomir.Flow cytometry was used to detect the apoptosis rate of nerve cells,and real-time fluorescence Quantitative PCR(Quantitative PCR)was performed Real-time PCR(q PCR)was used to detect the expression of miR-219a-5p in brain tissues.The expressions of target protein CACUL1 and apoptotic protein cleaved caspase-3 in rat brain tissues were detected by Western Blot.Results: Compared with the Sham group,the level of miR-219a-5p in the brain tissue of the TBI group was increased,and the CACUL1 was decreased,and the cleaved caspase-3protein was increased,and the cell apoptosis rate was increased(P<0.05),which proved that TBI induced apoptosis of nerve cells.Compared with the TBI group,miR-219a-5p content in the brain tissue of the Dex group was decreased,and CACUL1 was increased,and cleaved caspase-3 protein was decreased,and the apoptosis rate was decreased(P<0.05),which proved that Dex could reduce the apoptosis of nerve cells after TBI.Compared with the Dex group,the content of miR-219a-5p in the brain tissues of the Dex+miR-219a-5p antagomir group was decreased,and the CACUL1 was increased,and the cleaved caspase-3 protein was decreased,and the cell apoptosis rate was decreased(P<0.05),suggesting that the effect of Dex on the reduction of nerve cell apoptosis after TBI might be realized through the regulation of miR-219a-5p/CACUL1 pathway.Conclusions : Dex may reduce nerve cell apoptosis after TBI through miR-219a-5p/CACUL1 pathway.