标题:Protective effect of hyperoside against hydrogen peroxide-induced dysfunction and oxidative stress in osteoblastic MC3T3-E1 cells
作者:Qi, Xin-Chun; Li, Bo; Wu, Wen-Liang; Liu, Hai-Chun; Jiang, Yun-Peng
作者机构:[Qi, Xin-Chun] Peoples Hosp Yiyuan Cty, Dept Orthoped, Yiyuan, Peoples R China.; [Li, Bo] Xinwen Min Grp CO LTD, Cent Hosp, Dept Orthopaed, Xinwen, 更多
通讯作者:Jiang, YunPeng;Jiang, YP
通讯作者地址:[Jiang, YP]Shandong Univ, Qilu Hosp, Dept Orthoped, 107 Wenhua West Rd, Jinan 250012, Shandong, Peoples R China.
来源:ARTIFICIAL CELLS NANOMEDICINE AND BIOTECHNOLOGY
出版年:2020
卷:48
期:1
页码:377-383
DOI:10.1080/21691401.2019.1709851
关键词:Hyperoside; oxidative stress; MAPK signalling
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.
收录类别:EI;SCOPUS;SCIE
资源类型:期刊论文
原文链接:https://www.scopus.com/inward/record.uri?eid=2-s2.0-85077480282&doi=10.1080%2f21691401.2019.1709851&partnerID=40&md5=2c0bc854f72ea54405bc1952163d2987
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