期刊
JOURNAL OF VETERINARY SCIENCE
卷 16, 期 3, 页码 297-306出版社
KOREAN SOC VETERINARY SCIENCE
DOI: 10.4142/jvs.2015.16.3.297
关键词
apoptosis; cadmium; caspase; mitogen-activated protein kinase; osteoblasts
资金
- National Natural Science Foundation of China [31302058, 31172373]
- Priority Academic Program Development of Jiangsu Higher Education Institutions
- Graduate Innovation Project of Jiangsu Province
- Specialized Research Fund for the Doctoral Program of Higher Education, China [20113250110003]
Exposure to cadmium (Cd) induces apoptosis in osteoblasts (OBs); however, little information is available regarding the specific mechanisms of Cd-induced primary rat OB apoptosis. In this study, Cd reduced cell viability, damaged cell membranes and induced apoptosis in OBs. We observed decreased mitochondrial transmembrane potentials, ultrastructure collapse, enhanced caspase-3 activity, and increased concentrations of cleaved PARP, cleaved caspase-9 and cleaved caspase-3 following Cd treatment. Cd also increased the phosphorylation of p38-mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinases (ERK)1/2 and c-jun N-terminal kinase (INK) in OBs. Pretreatment with the caspase inhibitor, N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone, ERK1/2 inhibitor (U0126), p38 inhibitor (SB203580) and JNK inhibitor (SP600125) abrogated Cd-induced cell apoptosis. Furthermore, Cd-treated OBs exhibited signs of oxidative stress protection, including increased antioxidant enzymes superoxide dismutase and glutathione reductase levels and decreased formation of reactive oxygen species. Taken together, the results of our study clarified that Cd has direct cytotoxic effects on OBs, which are mediated by caspase- and MAPK pathways in Cd-induced apoptosis of OBs.
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