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Published on: March 23, 2019
Bone impairment caused by AlCl3 is associated with activation of the JNK apoptotic pathway mediated by oxidative
Xu Yang1, Kaiyuan Yu1, Haoran Wang1
1Key Laboratory of the Provincial Education Department of Heilongjiang for Common Animal Disease Prevention and Treatment, Northeast Agricultural University, Harbin 150030, China.
Abstract:
Exposure to aluminum (Al) inhibits bone formation, the principal mechanism possibly due to oxidative stress. However, little data is available that establishes the precise relationship. In this study, Wistar rats were exposed to 0 (GC), 0.4 (GL), 0.8 (GM) or 1.6 (GH) mg/L aluminum trichloride (AlCl3) in drinking water for 90 days, respectively. The concentrations of Al in serum and bone, serum markers of bone metabolism, bone mineral density (BMD) and body weight were measured. Histological changes within femurs were observed by H&E, ALP, and TRACP staining. Oxidative stress markers and JNK apoptotic pathway were detected in bone. The results indicate that AlCl3 exposure decreased BMD, numbers of ALP-positive osteoblasts and serum levels of bone formation markers (B-ALP, PICP and BGP), and caused damaged to the trabecular structure. Serum levels of bone resorption markers (TRACP-5b, CTX-I) and numbers of TRACP-positive osteoclasts increased in GL, but conversely, they decreased in GM and GH. In addition, AlCl3 caused oxidative stress, up-regulated expression of c-Jun and pro-apoptotic factors with increased p-JNK/JNK ratio and down-regulated expression of anti-apoptotic factor Bcl-2 in bone. Taken together, these results indicate that bone impairment caused by AlCl3 is associated with activation of the oxidative stress-mediated JNK apoptotic pathway.
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