Background

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. Methods 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. Results 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. Conclusion CHR exposure relieved OGD-evoked PC12 cell damage by elevating miR-216a expression and thereby activating of PI3 K/AKT and JAK2/STAT3 pathways.

中文翻译：

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大黄酚通过上调 miR-216a 保护 PC12 细胞免受氧葡萄糖剥夺诱发的损伤。

背景

脑卒中是指急性发作的神经功能缺损综合征。在这项研究中，我们试图探讨大黄酚 (CP) 在脑卒中中发挥其调节作用的潜在机制。方法在PC12细胞中进行OGD诱导，构建脑卒中模型。随后，利用CCK-8测定、蛋白质印迹、流式细胞术分别测定细胞活力、增殖和凋亡。qRT-PCR 用于检测 miR-216a 的表达水平。然后，进行细胞转染以改变 miR-216a 的表达。此外，还进行了实验以确定参与 PI3 K/AKT 和 JAK2/STAT3 通路的关键因子的表达，以探索潜在机制。结果OGD 诱导抑制细胞活力，同时促进细胞凋亡。此外，它增强了增殖相关的 p53、p21 和凋亡相关的 Bax 和 Cleaved-caspase-3 的表达，同时抑制了 Bcl-2 的表达。此外，CHR 暴露改善了 OGD 诱发的效应，并提高了 miR-216a 的表达，以及参与 PI3 K/AKT 和 JAK2/STAT3 通路的关键因子的表达。然而，miR-216a 沉默显着逆转了 CHR 暴露引发的影响。结论CHR暴露通过提高miR-216a表达从而激活PI3 K/AKT和JAK2/STAT3通路减轻OGD诱发的PC12细胞损伤。