Abstract
Ganoderic Acid A (GAA) is often applied for healing cardiovascular and cerebrovascular ailments, but the influences in cerebral ischemia injury are still hazy. The research delved into the functions of GAA in hypoxia-triggered impairment in PC12 cells. PC12 cells received hypoxia management for 12 hr, and subsequently, cell viability, migration, apoptosis, and correlative protein levels were assessed. After preprocessing with GAA, above cell behaviors were monitored again. The vector of microRNA (miR)-153 inhibitor was utilized for PC12 cell transfection to further explore the functions of miR-153 in hypoxia-impaired cells. Pathways of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) and mammalian target of rapamycin (mTOR) were investigated via executing western blot for uncovering the latent mechanism. Results revealed that hypoxia disposition triggered PC12 cells impairment via restraining cell viability and migration and accelerating apoptosis. However, GAA visibly mollified hypoxia-provoked impairment in PC12 cells. Interestingly, the enhancement of miR-153 triggered by GAA was observed in hypoxia-impaired PC12 cells. After miR-153 inhibitor transfection, the protective functions of GAA in hypoxia-impaired PC12 cells were dramatically inversed. Furthermore, GAA caused PI3K/AKT and mTOR activations via enhancement of miR-153 in hypoxia-impaired PC12 cells. The findings evinced that GAA exhibited the protective functions in PC12 cells against hypoxia-evoked impairment through activating PI3K/AKT and mTOR via elevating miR-153.