Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8547155 | Food and Chemical Toxicology | 2018 | 28 Pages |
Abstract
In reviewing the literature, the cellular mechanism of fluoride F-induced osteoblast OB cells apoptosis is diverse and perplexing, but detailed regulatory pathway, targets and role of extracellular Ca2+ remains still unclear. Hence, in the present study, we investigated the effects of F (9â¯mg/L F ion) and different Ca2+ (0.5, 1, 2, 4, 8â¯mmol/L) levels treatment on the proliferation rate of osteoblast cells, intracellular free Ca2+ ([Ca2+]i) and endoplasmic reticulum (ER) stress apoptosis pathway related gene levels of rabbit OB cells. Our results demonstrated that F exposure had a pronounced negative effect on osteoblast survival, further different Ca2+ levels treatment suggested that low concentration of Ca2+ (0.5-1â¯mmol/L) relieved the damaged effect, on the contrary, high concentration of Ca2+ (2-8â¯mmol/L) enhanced the effect. In addition, F significantly increased [Ca2+]i levels and the expression of ER stress-induced cell apoptosis pathway related genes. Treatment with 0.5-1â¯mmol/L Ca2+ markedly reversed the F-induced harmful effects, but high dose Ca2+ (2-8â¯mmol/L) enhanced these effects. In summary, 0.5-1â¯mmol/L Ca2+ can alleviate F-induced OB cells injure through ER stress apoptosis pathway, which provided a dose basis for the future study on the treatment of skeletal fluorosis with Ca2+.
Keywords
CaMKsRT-PCRHBSSPMSFFCSPVDFTBSTsodium dodecyl sulfate-polyacrylamide gelFBSDMEMPBSDABIntracellular free Ca2+DMSODulbecco's modified Eagle MediumF−Hanks balanced salt solution[Ca2+]iALPAlkaline phosphataseOsteoblastOsteoclastSDS-PAGEanalysis of varianceANOVAApoptosisdiaminobenzidineDimethylsulfoxidefetal bovine serumfetal calf serumendoplasmic reticulumFluoridephenylmethylsulfonyl fluoridePhosphate-buffered salinereverse transcription polymerase chain reactionCalcium
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Authors
Jinming Wang, Yangfei Zhao, Xiaofang Cheng, Yanyan Li, Huimiao Xu, Ram Kumar Manthari, Jundong Wang,