Lycium barbarum polysaccharides exert an antioxidative effect on rat chondrocytes by activating the nuclear factor (erythroid-derived 2)-like 2 signaling pathway

被引:7
作者
Chen, Yu [1 ]
Bi, Qing [1 ]
Zhu, Ziguan [2 ]
Zhang, Shuijun [1 ]
Xu, Jifeng [1 ]
Dou, Xiaofan [1 ]
Mao, Weihuan [3 ]
机构
[1] Hangzhou Med Coll, Zhejiang Prov Peoples Hosp, Dept Orthoped, Peoples Hosp, Hangzhou, Peoples R China
[2] Hangzhou Med Coll, Zhejiang Prov Peoples Hosp, Dept Hand Surg & Reconstruct Surg, Peoples Hosp, Hangzhou, Peoples R China
[3] Fifth Peoples Hosp Yuhang Dist, Dept Orthoped, Hangzhou, Peoples R China
关键词
Lycium barbarum polysaccharides; antioxidant; nuclear factor (erythroid-derived 2)-like 2 (Nrf2); osteoarthritis; DNA-DAMAGE; INDUCED APOPTOSIS; OXIDATIVE STRESS; OSTEOARTHRITIS; EXPRESSION; CELLS; PROLIFERATION; CONTRIBUTES; CANCER; NRF2;
D O I
10.5114/aoms.2018.77036
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Introduction: Oxidative stress is the main cause of osteoarthritis (OA). Lycium barbarum polysaccharides (LBP) have antioxidant properties. Thus, the potential effect of LBP on H2O2-stimulated chondrocytes was examined. Material and methods: The cell viability was detected by CCK-8. The reactive oxygen species (ROS) production and apoptosis rates were determined by flow cytometric analysis. The DNA damage was detected by comet assay. Real-time polymerase chain reaction (qPCR) and Western blot assays were performed to examine the expression of histone 2A family member X (gamma H2AX), checkpoint kinase 1 (Chk1), poly ADP-ribose polymerase (PARP), cysteinyl aspartate specific proteinase (caspase)-3/8/9, and nuclear factor (erythroid-derived 2)- like 2 (Nrf2) and its antioxidant-response element (ARE) dependent factors including heme oxygenase-1 (HO-1) and quinine oxidoreductase-1 (NQO-1). Results: Compared to the H2O2 group, LBP inhibited the ROS production and DNA damage caused by H2O2 (p < 0.05), respectively. LBP inhibited the mRNA and protein expressions of gamma H2AX and Chk1 (p < 0.05). Meanwhile, LBP significantly decreased apoptosis (p < 0.05). And LBP inhibited the expression levels of PARP and Caspase-3/ 8/9 (p < 0.05). Moreover, LBP increased the expression of Nrf2, HO-1 and NQO-1 (p < 0.05). Furthermore, the depletion of Nrf2 that mediated by RNA interference reversed the apoptosis and DNA damage inhibition effect of LBP (p < 0.05). Conclusions: LBP protected chondrocytes through inhibiting DNA damage and apoptosis caused by H2O2, in which the Nrf2/ARE signaling pathway played a positive role. It provided an inspiration for clinical application - developing LBP as a therapeutic agent and Nrf2 as a promising candidate.
引用
收藏
页码:964 / 973
页数:10
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