Chrysophanol protects PC12 cells against oxygen glucose deprivation-evoked injury by up-regulating miR-216a.

Cerebral stroke refers to an acute onset of neurological deficit syndrome. In this research, we attempted to probe into the underlying mechanisms by which chrysophanol (CP) performed its regulatory roles in cerebral stroke. OGD inducement was conducted in PC12 cells to construct a cerebral stroke model. Subsequently, CCK-8 assay, western blot, flow cytometry were utilized to determine cell viability, proliferation, and apoptosis, respectively. qRT-PCR was employed for detecting miR-216a expression level. Afterward, cell transfection was performed to alter miR-216a expression. Further, experiments were conducted to determine the expression of crucial factors participated in PI3 K/AKT and JAK2/STAT3 pathways for exploring the underlying mechanisms. OGD inducement suppressed cell viability, while promoted cell apoptosis. Besides, it enhanced the expression of proliferation-associated p53, p21, and apoptosis-associated Bax, and Cleaved-caspase-3, while suppressed the expression of Bcl-2. Furthermore, CHR exposure ameliorated the effects that OGD-evoked, and elevated the expression of miR-216a, as well as the expression of crucial factors participated in PI3 K/AKT and JAK2/STAT3 pathways. However, miR-216a silencing markedly reversed the effects triggered by CHR exposure. CHR exposure relieved OGD-evoked PC12 cell damage by elevating miR-216a expression and thereby activating of PI3 K/AKT and JAK2/STAT3 pathways.