Circular RNA ACR relieves high glucose-aroused RSC96 cell apoptosis and autophagy via declining microRNA-145-3p.

Recently, the impacts of noncoding RNAs on the initiation and development of diabetic peripheral neuropathy (DPN) have aroused wide attention. Herein, we tested the impacts of autophagy-related circular RNA (ACR) on in vitro cell model of DPN. Rat Schwann RSC96 cells underwent high glucose (HG) irritation. The ACR expression, cell viability, apoptosis, autophagy, and reactive oxygen species (ROS) generation were tested, respectively. Exogenous PLCDH-ACR transfection was utilized for probing the impacts of ACR on HG-irritated Schwann cells 96 (RSC96). Then, whether microRNA-145-3p (miR-145-3p) attended to the impacts of ACR on HG-irritated RSC96 cells was measured. Finally, the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway activity was evaluated. HG lowered ACR expression in RSC96 cells. Exogenous PLCDH-ACR transfection relieved HG-aroused RSC96 cell apoptosis, autophagy and ROS generation. Moreover, exogenous PLCDH-ACR transfection declined miR-145-3p expression in HG-irritated RSC96 cells. miR-145-3p engaged in the impacts of ACR on HG-aroused RSC96 cell apoptosis, autophagy, and ROS generation. Besides, exogenous PLCDH-ACR transfection promoted PI3K/AKT/mTOR pathway activation in HG-irritated RSC96 cells through declining miR-145-3p expression. This study disclosed that ACR relieved HG-aroused RSC96 cell apoptosis, autophagy and ROS generation might be via declining miR-145-3p and then promoting PI3K/AKT/mTOR pathway activation.