Protective effect of hyperoside against hydrogen peroxide-induced dysfunction and oxidative stress in osteoblastic MC3T3-E1 cells

被引:29
作者
Qi, Xin-Chun [1 ]
Li, Bo [2 ]
Wu, Wen-Liang [3 ]
Liu, Hai-Chun [3 ]
Jiang, Yun-Peng [3 ]
机构
[1] Peoples Hosp Yiyuan Cty, Dept Orthoped, Yiyuan, Peoples R China
[2] Xinwen Min Grp CO LTD, Cent Hosp, Dept Orthopaed, Xinwen, Peoples R China
[3] Shandong Univ, Qilu Hosp, Dept Orthoped, 107 Wenhua West Rd, Jinan 250012, Shandong, Peoples R China
关键词
Hyperoside; oxidative stress; MAPK signalling; P38; MAPK; BONE; NRF2/HO-1; APOPTOSIS; PATHWAY; DAMAGE; JNK;
D O I
10.1080/21691401.2019.1709851
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Oxidative stress can induce apoptosis and decrease activities of osteoblasts. Hyperoside (HYP) is a potent antioxidant derived from Chinese herb. This study aims to evaluate the protective effects provided by HYP to osteoblastic MC3T3-E1 cells. MC3T3-E1 cells were pre-treated with HYP for 24 h before being treated with 0.3 mM hydrogen peroxide (H2O2) for 24 h. Cell viability, flow cytometric analysis and mRNA expression of alkaline phosphatase (ALP), collagen I (COL-I) and osteocalcin (OCN) in MC3T3-E1 cells were examined. We next examined apoptosis-related and mitogen-activated protein kinase (MAPK) related proteins in HYP and H2O2 groups. HYP over the dose of 40 mu mol/L could obviously increase the MC3T3-E1 cell viability at 24 h and 48 h (p < .05). HYP significantly (p < .05) increased mRNA expression of ALP, COL-I and OCN than H2O2 group. Moreover, HYP decreased the apoptosis rate and apoptosis-related proteins that induced by H2O2. In addition, HYP decreased the production of phosphorylated Jun N-terminal kinase (JNK) and p38 levels of osteoblastic MC3T3-E1 cells induced by H2O2. These results demonstrated that the protective effect provided by HYP to osteoblastic MC3T3-E1 cells was mediated, at least in part, via inhibition of MAPK signalling pathway and oxidative damage of the cells.
引用
收藏
页码:377 / 383
页数:7
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