MiR‐92b‐3p regulates oxygen and glucose deprivation–reperfusion‐mediated apoptosis and inflammation by targeting TRAF3 in PC12 cells

New Findings What is the central question of this study? MiR‐92b‐3p was found to be reduced in a rat model of middle cerebral artery occlusion: what are the functions of miR‐92b‐3p in oxygen and glucose deprivation–reperfusion (OGD/R)? What is the main finding and its importance? MiR‐92b‐3p abated apoptosis, mitochondrial dysfunction and inflammation caused by OGD/R via targeting TRAF3, suggesting that miR‐92b‐3p may serve as a potential therapeutic target in ischaemic stroke treatment. Abstract Stroke is the most common cause of human neurological disability. MiR‐92b‐3p has been shown to be decreased in a rat model of middle cerebral artery occlusion, but its effects in cerebral ischaemic insult are unknown. In this study, PC12 cells were exposed to oxygen and glucose deprivation–reperfusion (OGD/R) to establish cerebral ischaemic injury in vitro . Quantitative real time‐PCR analysis demonstrated that OGD/R exposure led to down‐regulation of miR‐92b‐3p and increased mRNA and protein levels of tumour necrosis factor receptor‐associated factor 3 (TRAF3). Gain of miR‐92b‐3p expression facilitated cell survival; attenuated lactate dehydrogenase leakage, cell apoptosis, caspase 3 activity and cleaved‐caspase 3 (c‐caspase 3) expression; and decreased the Bax/Bcl‐2 ratio. Furthermore, miR‐92b‐3p repressed mitochondrial membrane potential depolarization, reactive oxygen species production, cytochrome c protein expression, inflammatory cytokine production and the reduction of ATP content. MiR‐92b‐3p directly targeted the 3ʹ‐untranslated region of TRAF3 and decreased TRAF3 expression. Reinforced expression of TRAF3 partly abrogated the biological activity of miR‐92b‐3p during OGD/R. Hence, miR‐92b‐3p abated apoptosis, mitochondrial dysfunction and inflammatory responses induced by OGD/R by targeting TRAF3.