Zinc Inhibits High Glucose-Induced Apoptosis in Peritoneal Mesothelial Cells

被引：17

作者：

Zhang, Xiuli ^{[1
,2
]}

Liang, Dan ^{[3
,4
]}

Guo, Baolei ^{[3
]}

Yang, Lina ^{[1
]}

Wang, Lining ^{[1
]}

Ma, Jianfei ^{[1
]}

机构：

[1] China Med Univ, Dept Nephrol, Affiliated Hosp 1, Shenyang 110001, Liaoning, Peoples R China

[2] Benxi Railway Hosp, Dept Nephrol, Benxi, Liaoning, Peoples R China

[3] China Med Univ, Dept Orthoped, Affiliated Hosp 1, Shenyang 110001, Liaoning, Peoples R China

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

来源：

BIOLOGICAL TRACE ELEMENT RESEARCH | 2012年 / 150卷 / 1-3期

关键词：

Rat peritoneal mesothelial cells; Zinc; High glucose; Apoptosis; RECEPTOR-MEDIATED APOPTOSIS; OXIDATIVE STRESS; MESENCHYMAL TRANSITION; DIALYSIS SOLUTIONS; TRACE-ELEMENTS; DEATH; PROTEINS; PATHWAY; HEMODIALYSIS; MEMBRANE;

D O I：

10.1007/s12011-012-9473-y

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 (Zn) plays an important role in influencing many types of apoptosis. However, its function in apoptosis in peritoneal mesothelial cells (PMCs) remains unknown. Here, we studied the effects of Zn on high glucose (HG)-induced apoptosis in rat PMCs (RPMCs) and examined the underlying molecular mechanisms. We found that Zn supplementation inhibited HG-induced RPMC apoptosis significantly, by attenuating reactive oxygen species (ROS) production, inhibiting HG-induced sFasR and sFasL over-expression, caspase-8 and caspase-3 activation, and inhibiting release of cytochrome c from mitochondria to the cytosol. Further analysis revealed that Zn supplementation facilitated cell survival through activation of the phosphatidylinositol 3-kinase/Akt signaling pathway and MAPK/ERK pathways. These results indicate that Zn can inhibit apoptosis in HG-induced RPMCs by several independent mechanisms, including an indirect antioxidative effect and probably by inhibition of caspase-8 and caspase-3 activation.

引用

页码：424 / 432

页数：9

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