关键词: microRNA-126-5p, 糖氧剥夺再灌注, 肿瘤坏死因子受体相关因子 3, 细胞凋亡, 炎症, 神经元

Abstract: Objective To explore the effect of miR-126-5p on apoptosis and inflammatory response in mouse hippocampal neuron HT22 cells mediated by oxygen-glucose deprivation / reperfusion (OGD / R) by targeting tumor necrosis factor receptor-associated factor 3 (TRAF3). Methods The OGD / R cell model was established in vitro by simulating ischemia / reperfusion (I / R) injury. The targeting relationship between miR-126-5p and TRAF3 and the effect of miR-126-5p on apoptosis and inflammatory response in HT22 cells were analyzed. Results The level of miR-126-5p inthe OGD / R group was down-regulated while the mRNA and expression levels of TRAF3 were upregulated when compared with those in the control group. The cell survival rate and the Bcl-2 expression level in the OGD / R group were decreased while the lactate dehydrogenase ( LDH) release, the apoptosis rate and the protein expression levels of Bax and cleaved caspase-3 in the OGD / Rgroup were increased when compared with those in the control group (all P< 0. 05). The protein expression levels of TRAF3, Bax and cleaved caspase-3, the LDH release, the apoptosis rate were significantly decreased in the OGD / R + miR-mimic group and the OGD + miR-mimic + pcDNA group while the cell survival rate and the protein expression level of Bcl-2 were increased when compared with those in the OGD / R + mimic-NC group. In addition, the above indicators were elevated in the OGD + miR-mimic + pcDNA-TRAF3 group while the cell survival rate was significantly lowered when compared with those in the OGD/R+mimic-NC group (all P<0.05). Conclusion  miR-126-5p can inhibit the OGD/R-mediated apoptosis of and inflammatory response in HT22 cells by targeting TRAF3, thus playing a protective role on neuronal cells.

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