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芒果苷减轻IL-1β诱导的软骨细胞凋亡
引用本文:朱鹏,刘琮,李博,赵晨,周涛,薛欣,张兵.芒果苷减轻IL-1β诱导的软骨细胞凋亡[J].中南大学学报(医学版),2021,46(1):25-31.
作者姓名:朱鹏  刘琮  李博  赵晨  周涛  薛欣  张兵
作者单位:西安医学院第二附属医院骨外科,西安 710038
基金项目:陕西省社会发展科技攻关项目(2016SF-017);陕西省教育厅专项科研计划项目(16JK1663)。
摘    要:目的:软骨细胞凋亡是骨关节炎重要的发病机制,芒果苷具有抗炎和抗凋亡等多种药理作用,然而芒果 苷对软骨细胞凋亡的作用尚不清楚。本研究探讨芒果苷对IL-1β诱导的软骨细胞凋亡的影响。方法:将小鼠软骨细胞 ATDC5随机分为control组、IL-1β组、MFN-L组、MFN-M组、MFN-H组及MFN+LY294002组。Control组细胞不加 任何干预;IL-1β组细胞用IL-1β(10 ng/mL)处理24 h;MFN-L、MFN-M、MFN-H组细胞先分别用5、10、20 μmol/L 的芒果苷预处理 1 h,再用 IL-1β(10 ng/mL)处理 24 h;MFN+LY294002 组细胞先加入 LY294002(25 μmol/L)处理 1 h, 再加入芒果苷(20 μmol/L)处理1 h,最后再用IL-1β(10 ng/mL)处理24 h。用CCK-8检测细胞活力,流式细胞术检测细 胞凋亡,比色法检测caspase-3活性,蛋白质印迹法检测Bcl-2,Bax及磷脂酰肌醇-3-激酶/蛋白激酶B(PI3K/Akt)通路 相关蛋白质的表达。结果:与control组相比,IL-1β组细胞活力显著降低,细胞凋亡率显著上升,caspase-3活性显著 增加,Bax蛋白质表达水平显著上调,Bcl-2、p-PI3K和p-Akt蛋白质表达水平显著下调(均P<0.05)。与IL-1β组相比, MFN-L、MFN-M、MFN-H组细胞活力显著升高,细胞凋亡率显著下降,caspase-3活性显著下降,Bax蛋白质表达水 平显著下调,Bcl-2、p-PI3K和p-Akt蛋白质表达水平显著上调(均P<0.05)。与MFN-M组相比,MFN+LY294002组细 胞凋亡率显著上升,Bax蛋白质表达水平显著上调,Bcl-2蛋白质表达水平显著下调(均P<0.05)。结论:芒果苷可减 轻IL-1β诱导的软骨细胞凋亡,其保护作用是通过激活PI3K/Akt通路实现的。


Mangiferin attenuates IL-1β-induced chondrocytes apoptosis
ZHU Peng,LIU Cong,LI Bo,ZHAO Chen,ZHOU Tao,XUE Xin,ZHANG Bing.Mangiferin attenuates IL-1β-induced chondrocytes apoptosis[J].Journal of Central South University (Medical Sciences)Journal of Central South University (Medical Sciences),2021,46(1):25-31.
Authors:ZHU Peng  LIU Cong  LI Bo  ZHAO Chen  ZHOU Tao  XUE Xin  ZHANG Bing
Affiliation:Department of Orthopedics, Second Affiliated Hospital of Xi’ an Medical University, Xi’ an 710038, China
Abstract:Objective: Chondrocyte apoptosis is an important process in the pathogenesis of osteoarthritis. Mangiferin exerts multiple pharmacological effects such as anti inflammatory and anti-apoptosis. However, the role of mangiferin in chondrocyte apoptosis is not clear. In this study, we aimed to explore the role of mangiferin in IL-1β -induced chondrocyte apoptosis. Methods: ATDC5 cells were randomly divided into a control group, a IL-1β group, a MFN L group, a MFN-M group, a MFN-H group and a MFN+LY294002 group. Cells in the control group were treated with IL-1β (10 ng/mL) for 24 h; cells in the MFN-L group, the MFN-M group and the MFN-H group were pretreated with 5, 10 and 20 μmol/L mangiferin for 1 h respectively, and then they were treated with IL-1β (10 ng/mL) for 24 h; cells in the MFN+LY294002 group were treated with LY294002 (25 μmol/L) for 1 h, then mangiferin (20 μmol/L) and IL-1β (10 ng/mL) for 1 h and 24 h, respectively. Cell viability was detected by CCK-8 assay and cell apoptosis was measured by flow cytometry. Colorimetric assay was conducted to measure the caspase-3 activity. The protein levels of Bcl-2, Bax, and phosphoinositide 3-kinase (PI3K)/Akt signaling pathway related proteins were detected by Western blotting. Results: Compared to the control group, cell viability was significantly decreased; cell apoptosis, caspase-3 activity and Bax protein expression were significantly increased; the protein levels of Bcl-2, p-PI3K, and p-Akt were significantly decreased in the IL-1β group (all P<0.05). Compared to the IL-1β group, cell viability was significantly increased; cell apoptosis, caspase-3 activity and Bax protein expression were significantly decreased; the protein levels of Bcl-2, p-PI3K, and p-Akt were significantly increased in the MFN-L, the MFN-M and the MFN-H groups (all P<0.05). Compared to the MFN-M group, cell apoptosis and the protein level of Bax in the MFN+LY294002 group were significantly increased; the Bcl-2 protein expression was significantly decreased (all P<0.05). Conclusion: Mangiferin could attenuate IL-1β-induced apoptosis of the mice chondrocytes, which is mediated by the activation of PI3K/Akt signaling pathway.
Keywords:osteoarthritis  mangiferin  IL-1β  chondrocyte  apoptosis  phosphoinositide 3-kinase/Akt  
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