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| miR-214-3p调控PI3K/AKT通路对软骨细胞自噬和凋亡的影响 |
| Effects of miR-214-3p on autophagy and apoptosis of chondrocytes through regulation of PI3K/AKT pathway |
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| DOI：10.3969/j.issn.1006-7108.2024.11.001 |
| 中文关键词: miR-214-3p 骨关节炎 软骨细胞 自噬 凋亡 PI3K/AKT通路 |
| 英文关键词:miR-214-3p osteoarthritis chondrocyte autophagy apoptosis PI3K/AKT pathway |
| 基金项目:湖北省自然科学基金（2021CFB217） |
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| 中文摘要: |
| 目的 探讨miR-214-3p对IL-1β诱导的软骨细胞自噬和凋亡的影响及其可能的机制。方法 采用10 ng/mL的IL-1β诱导大鼠关节软骨细胞24 h，构建骨关节炎（osteoarthritis, OA）细胞模型，将细胞分为对照组、模型组、miR-NC组、miR-214-3p mimics组、740Y-P（PI3K/AKT通路激活剂）+miR-214-3p mimics组和LY294002（PI3K/AKT通路抑制剂）+miR-214-3p mimics组。通过CCK8检测细胞活力、流式细胞术检测细胞凋亡、透射电镜观察细胞中的自噬小体、Western blot检测凋亡（Bcl-2、Bax）、自噬（LC3II、Beclin-1）和PI3K/AKT通路（AKT、p-AKT）相关蛋白的表达。结果 与对照组相比，模型组细胞活力降低（P<0.01），细胞凋亡率升高（P<0.01），自噬小体明显减少，细胞中Bcl-2、LC3II和Beclin-1蛋白表达水平降低（P<0.01），Bax和p-AKT/AKT水平升高（P<0.01）；与miR-NC组相比，miR-214-3p mimics组细胞活力升高（P<0.01），细胞凋亡率降低（P<0.01），自噬小体明显增多，细胞中Bcl-2、LC3II和Beclin-1蛋白表达水平升高（P<0.01），Bax和p-AKT/AKT水平降低（P<0.01）；与miR-214-3p mimics单独作用相比，联合740Y-P能够逆转miR-214-3p mimics的上述作用，而联合LY294002能够进一步加重miR-214-3p mimics的上述作用。结论 miR-214-3p能够促进OA细胞增殖和自噬，并抑制细胞凋亡，其机制可能与抑制PI3K/AKT通路的激活有关。 |
| 英文摘要: |
| Objective To investigate the effects of miR-214-3p on chondrocyte autophagy and apoptosis induced by IL-1β and its possible mechanism. Methods Rat articular chondrocytes were induced by 10 ng/mL IL-1β for 24 h, to establish osteoarthritis (OA) cell model. The cells were divided into control group, model group, miR-NC group, miR-214-3p mimics group, 740Y-P (PI3K/AKT pathway activator) +miR-214-3p mimics group, and LY294002 (PI3K/AKT pathway inhibitor) +miR-214-3p mimics group. Cell viability was detected with CCK8. Cell apoptosis was detected with flow cytometry. Autophagosomes in cells were observed using transmission electron microscopy. Expressions of apoptosis (Bcl-2, Bax), autophagy (LC3II, Beclin-1), and PI3K/AKT pathway (AKT, p-AKT) related proteins were detected using Western blotting. Results Compared to those in the control group, the cell viability in the model group decreased (P<0.01), the apoptosis rate increased (P<0.01), autophagosomes decreased, the expression levels of Bcl-2, LC3II, and Beclin-1 proteins decreased (P<0.01), and Bax and p-AKT/AKT levels increased (P<0.01). Compared to those in the miR-NC group, cell viability in miR-214-3p mimics group increased (P<0.01), the apoptosis rate decreased (P<0.01), autophagosomes increased, the expression levels of Bcl-2, LC3II and Beclin-1 proteins increased (P<0.01), and Bax and p-AKT/AKT levels decreased (P<0.01). Compared to those in the effects of miR-214-3p mimics alone, the combination of 740Y-P reversed the above effects of miR-214-3p mimics, while the combination of LY294002 further aggravated the above effects of miR-214-3p mimics. Conclusion miR-214-3p promotes OA cell proliferation and autophagy, and inhibits apoptosis, which may be related to the inhibition of the activation of PI3K/AKT pathway. |
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