Dexmedetomidine promotes cell proliferation and inhibits cell apoptosis by regulating LINC00982 and activating the phosphoinositide-3-kinase (PI3K)/protein kinase B (AKT) signaling in hypoxia/reoxygenation-induced H9c2 cells

Previous studies showed dexmedetomidine (DEX) could alleviate myocardial ischemia/reperfusion injury (MIRI). Nevertheless, the mechanisms by which DEX alleviated MIRI remain to be determined. Our results demonstrated that DEX reversed hypoxia/reoxygenation (H/R)-induced decreased proliferation, and enhanced LINC00982 level, apoptosis, and inflammation in H9c2 cells. Moreover, LINC00982 overexpression attenuated the DEX-mediated protective effect of H9c2 cells under H/R. In addition, DEX upregulated p-phosphoinositide-3-kinase (p-PI3K) and p-protein kinase B (p-AKT) levels, and the silencing of LINC00982 further enhanced this effect in H/R-induced H9c2 cells. Furthermore, LINC00982 deletion enhanced the protective effect of DEX on H9c2 cells under H/R condition, while PI3K inhibitor, LY294002, obviously reversed this phenomenon. In sum, our work determined that DEX could suppress cell apoptosis and inflammation in H/R-triggered H9c2 through downregulating LINC00982 and activating PI3K/AKT signaling.