Zinc Inhibits H2O2-Induced MC3T3-E1 Cells Apoptosis via MAPK and PI3K/AKT Pathways

被引：74

作者：

Liang, Dan ^{[1
,2
]}

Yang, Maowei ^{[1
]}

Guo, Baolei ^{[1
]}

Cao, Junjun ^{[1
]}

Yang, Lei ^{[1
]}

Guo, XiaoDong ^{[1
]}

Li, Yuanzhou ^{[1
]}

Gao, Zhida ^{[1
]}

机构：

[1] China Med Univ, Affiliated Hosp 1, Dept Orthoped, Shenyang, Liaoning, Peoples R China

[2] Troops 95935 Unit, Haerbin, Heilongjiang, Peoples R China

来源：

BIOLOGICAL TRACE ELEMENT RESEARCH | 2012年 / 148卷 / 03期

基金：

中国国家自然科学基金;

关键词：

Zinc; H2O2; PI3K/Akt; ERK; P38; JNK; KAPPA-B ACTIVATION; OXIDATIVE STRESS; SIGNALING PATHWAY; PHOSPHATASE ACTIVITY; DIETARY ZINC; SUPPLEMENTATION; PROLIFERATION; EXPRESSION; OSTEOBLAST; PROTECTS;

D O I：

10.1007/s12011-012-9387-8

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Zinc has been shown to increase bone mass and promote bone cell proliferation and differentiation. We, therefore, hypothesized that zinc might be cytoprotective for bone cells during oxidative stress. The cells were divided into H2O2, zinc and zinc + H2O2 groups. In the present study, zinc was found to inhibit H2O2-induced apoptosis in MC3T3-E1 cells, as shown by analysis of Annexin V/PI double staining. Western blot data showed that in zinc + H2O2-treated cells, zinc decreased the levels of AIF, Bax and active caspase-9 and -3, which are pro-apoptotic factors. And zinc inhibited release of cytochrome c from mitochondria to cytosol in zinc + H2O2-treated cells. Further investigation shows that protection is via activation of PI3K/Akt/mTor and MAPK /ERK pathways and inhibition of MAPK/P38 and MAPK/JNK pathways. Protecting osteoblast cells from oxidative damage presents a potential application in the treatment of osteoporosis.

引用

页码：420 / 429

页数：10

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