中国骨质疏松杂志

钩藤碱通过Nrf2/HO-1信号通路抑制IL-1β诱导的软骨细胞损伤

Rhynchophylline inhibits IL-1β-induced chondrocyte damage through Nrf2/HO-1 signaling pathway

DOI：10.3969/j.issn.1006-7108.2023.07.006

中文关键词: 钩藤碱 NF-E2相关因子2 血红素氧合酶1 软骨细胞白介素1β

英文关键词:rhynchophylline nuclear factor erythroid 2-related factor 2 heme oxygenase-1 chondrocyte interleukin-1β

基金项目:河南省中医药科学研究专项课题（2019ZYBJ18）

作者	单位
王西彬1 左瑞庭2* 王新立1 李浩亮1 刘汝银1	1.河南省中医院·河南中医药大学第二附属医院脊柱科，河南郑州 450002 2.河南省中医院·河南中医药大学第二附属医院风湿科，河南郑州 450002

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中文摘要:

目的探讨钩藤碱对IL-1β诱导的软骨细胞凋亡、氧化应激和炎症等损伤的影响及其分子机制。方法将大鼠软骨细胞分为对照组、IL-1β（10 ng/mL）组、IL-1β+钩藤碱（5、25、50 μmol/L）组；MTT实验检测钩藤碱对细胞活力的影响；Western blot方法检测Bcl2、Bax、MMP3、MMP13、Collagen Ⅱ、Nrf2和HO-1蛋白水平；ELISA方法检测炎性因子PGE2、COX-1、TNF-α和ROS水平；试剂盒检测MDA水平。结果与对照组相比，IL-1β组细胞活力明显抑制（P＜0.05）；与IL-1β组相比，钩藤碱25 μmol/L组和50 μmol/L组细胞活力增强（P＜0.05）。与对照组相比，IL-1β组Bcl2蛋白表达减少，Bax蛋白表达增加（P＜0.05）；与IL-1β组相比，钩藤碱25 μmol/L组和50 μmol/L组Bcl2蛋白表达增加，钩藤碱50 μmol/L组Bax蛋白表达减少（P＜0.05）。与对照组相比，IL-1β组MMP13和MMP3蛋白表达上调，Collagen Ⅱ蛋白表达下调（P＜0.05）；与IL-1β组相比，钩藤碱5、25和50 μmol/L组MMP13和MMP3蛋白表达降低，钩藤碱25 μmol/L组和50 μmol/L组Collagen Ⅱ蛋白表达增加（P＜0.05）。与对照组相比，IL-1β组PGE2、COX-1、TNF-α、ROS和MDA水平均升高（P＜0.05）；与IL-1β组相比，钩藤碱25 μmol/L组和50 μmol/L组PGE2、COX1、TNF-α、ROS和MDA水平均降低（P＜0.05）。与对照组相比，IL-1β组Nrf2和HO-1蛋白表达减少（P＜0.05）；与IL-1β组相比，钩藤碱25 μmol/L组和50 μmol/L组Nrf2和HO-1蛋白表达增加（P＜0.05）。结论钩藤碱通过激活Nrf2/HO-1信号通路抑制IL-1β诱导的软骨细胞凋亡、氧化应激和炎症等损伤。

英文摘要:

Objective To explore the effects of rhynchophylline on the oxidative stress and inflammatory injuries in IL-1β-induced chondrocytes. Methods The rat chondrocytes were divided into control group, IL-1β (10 ng/mL) group, and IL-1β+rhynchophylline (5, 25, 50 μmol/L) groups. The effect of rhynchophylline on cell viability was detected with MTT. The protein levels of Bcl2, Bax, MMP3, MMP13, collagen II, Nrf2, and HO-1 were detected with Western Blotting. The levels of inflammatory cytokines PGE2, COX-1, TNF-α, and ROS were detected with ELISA. The level of MDA was used to detected with a kit. Results Compared to that in the control group, cell viability was repressed in IL-1β group (P<0.05). Compared to that in IL-1β group, cell viability increased in rhynchophylline (25 μmol/L and 50 μmol/L) groups (P<0.05). Compared to those in the control group, Bcl2 protein expression decreased and Bax protein expression elevated in IL-1β group (P<0.05). Compared to those in IL-1β group, Bcl2 protein expression increased in rhynchophylline (25 μmol/L and 50 μmol/L) groups and Bax protein expression was inhibited in rhynchophylline (50 μmol/L) group (P<0.05). Compared to those in the control group, MMP13 and MMP3 protein levels were up-regulated and collagen II protein expression was down-regulated in IL-1β group (P<0.05). Compared to those in IL-1β group, MMP13 and MMP3 protein expression reduced in rhynchophylline (5 μmol/L, 25 μmol/L and 50 μmol/L) groups and collagen II protein expression was enhanced in rhynchophylline (25 μmol/L and 50 μmol/L) groups (P<0.05). Compared to those in the control group, the levels of PGE2, COX1, TNF-α, ROS, and MDA were promoted in IL-1β group (P<0.05). Compared to those in IL-1β group, the levels of PGE2, COX-1, TNF-α, ROS, and MDA were diminished in rhynchophylline (25 μmol/L and 50 μmol/L) groups (P<0.05). Compared to those in the control group, Nrf2 and HO-1 protein expression were reduced in IL-1β group (P<0.05). Compared to those in IL-1β group, Nrf2 and HO-1 protein expression increased in rhynchophylline (25 μmol/L and 50 μmol/L) groups (P<0.05). Conclusion Rhynchophylline inhibits IL-1β-induced oxidative stress and inflammatory damage in chondrocytes by activating Nrf2/HO-1 signaling pathway.

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