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引用本文:杨波,龙慧,王郑钢,曾德辉,张彬,龙秋平.白藜芦醇激活Nrf-2信号抑制H2O2诱导的骨关节炎软骨细胞凋亡、氧化损伤和炎症反应[J].中国现代应用药学,2021,38(19):2359-2366.
YANG Bo,LONG Hui,WANG Zhenggang,ZENG Dehui,ZHANG Bin,LONG Qiuping.Resveratrol Activates Nrf-2 Signal to Inhibit Apoptosis, Oxidative Damage and Inflammatory Response of Osteoarthritis Chondrocyte Induced by H2O2[J].Chin J Mod Appl Pharm(中国现代应用药学),2021,38(19):2359-2366.
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白藜芦醇激活Nrf-2信号抑制H2O2诱导的骨关节炎软骨细胞凋亡、氧化损伤和炎症反应
杨波1, 龙慧2, 王郑钢1, 曾德辉1, 张彬1, 龙秋平1
1.南华大学附属南华医院骨科, 湖南 衡阳 421002;2.南华大学附属第二医院疼痛康复科, 湖南 衡阳 421001
摘要:
目的 研究白藜芦醇在H2O2诱导骨关节炎软骨细胞凋亡、氧化损伤和炎症反应中的作用。方法 通过MTT试验检测H2O2和(或)白藜芦醇处理原代软骨细胞增殖活性,流式细胞仪检测细胞凋亡情况;通过实时定量荧光PCR和Western blotting检测各处理组Nrf2-HO-1/NQO-1信号因子,抗氧化酶基因SOD-2、GPx4和CAT,炎症信号因子NF-κB、COX-2和iNOS的表达水平;流式细胞仪检测细胞ROS水平和脂质氧化水平;ELISA检测各处理组细胞炎症因子IL-6、IL-8、TNF-α的释放情况。结果 白藜芦醇能够恢复H2O2诱导的原代软骨细胞凋亡,增加细胞增殖活性;上调Nrf2-HO-1/NQO-1信号因子和抗氧化酶基因SOD-2、GPx4和CAT的表达,降低H2O2诱导的ROS和脂质氧化水平;降低H2O2诱导的炎症信号因子NF-κB、COX-2和iNOS的表达水平,降低炎症因子IL-6、IL-8、TNF-α的释放。结论 白藜芦醇可能通过增加转录因子Nrf-2的激活以及其直接抗氧化和抗炎作用来发挥对软骨细胞的保护作用,以改善骨关节炎的氧化损伤和炎症反应。
关键词:  白藜芦醇  骨关节炎  软骨细胞  H2O2  Nrf-2
DOI:10.13748/j.cnki.issn1007-7693.2021.19.004
分类号:R285.5
基金项目:湖南省卫健委科研计划项目(C2019101);衡阳市科技局指导项目(S2018F9031022230)
Resveratrol Activates Nrf-2 Signal to Inhibit Apoptosis, Oxidative Damage and Inflammatory Response of Osteoarthritis Chondrocyte Induced by H2O2
YANG Bo1, LONG Hui2, WANG Zhenggang1, ZENG Dehui1, ZHANG Bin1, LONG Qiuping1
1.Department of Orthopedics, The Affiliated Nanhua Hospital of Nanhua University, Hengyang 421002, China;2.Department of Pain Rehabilitation, The Second Affiliated Hospital of Nanhua University, Hengyang 421001, China
Abstract:
OBJECTIVE To investigate the role of resveratrol on apoptosis, oxidative damage and inflammatory response of osteoarthritis chondrocytes induced by H2O2. METHODS MTT assay was used to detect the proliferation of primary chondrocyte treated with H2O2 and/or resveratrol, and flow cytometry was used to detect the apoptosis of chondrocyte. The expression levels of Nrf2-HO-1/NQO-1 signal factor, antioxidant enzyme gene SOD-2, GPx4 and CAT, inflammatory signal factor NF-κB, COX-2 and iNOS were detected by real-time quantitative fluorescence PCR and Western blotting. Flow cytometry was used to detect the level of ROS and lipid oxidation. The release of inflammatory cytokines IL-6, IL-8 and TNF-α in each treatment group was detected by ELISA. RESULTS Resveratrol could restore the apoptosis of primary chondrocyte induced by H2O2and increase the proliferation activity of chondrocyte; upregulate the expression of Nrf2-HO-1/NQO-1 signal factor and antioxidant gene SOD-2, GPx4 and CAT, and reduce the ROS and lipid oxidation level induced by H2O2; reduce the expression of inflammatory signaling factors NF-κB, COX-2 and iNOS induced by H2O2, and decrease the release of inflammatory factors IL-6, IL-8 and TNF-α. CONCLUSION Resveratrol may play a protective role on chondrocyte by increasing the activation of transcription factor Nrf-2 and its direct antioxidant and anti-inflammatory effects in order to improve the oxidative damage and inflammatory response of osteoarthritis.
Key words:  resveratrol  osteoarthritis  chondrocyte  H2O2  Nrf-2
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