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 (9 mg/L F ion) and different Ca²⁺ (0.5, 1, 2, 4, 8 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⁺ (0.5–1 mmol/L) relieved the damaged effect, on the contrary, high concentration of Ca²⁺ (2–8 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 0.5–1 mmol/L Ca²⁺ markedly reversed the F-induced harmful effects, but high dose Ca²⁺ (2–8 mmol/L) enhanced these effects. In summary, 0.5–1 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⁺.

在回顾文献中，氟化物F诱导的成骨OB细胞凋亡的细胞机制是多种多样的和令人困惑的，但细胞外Ca ^2+的详细调节途径，靶标和作用仍不清楚。因此，在本研究中，我们研究了F（9 mg / LF离子）和不同Ca ²⁺（0.5、1、2、4、8 mmol / L）处理对成骨细胞，细胞内增殖速率的影响。游离Ca ²⁺（内[Ca ²⁺ ] i）和兔OB细胞的内质网（ER）应力凋亡途径相关基因的水平。我们的结果表明F暴露对成骨细胞的存活有明显的负面影响，进一步不同的Ca ²⁺水平处理表明低浓度的Ca²⁺（0.5-1 mmol / L）减轻了损伤的作用，相反，高浓度的Ca ²⁺（2-8 mmol / L）增强了作用。此外，F显着增加了[Ca ²⁺ ] i水平和内质网应激诱导的细胞凋亡途径相关基因的表达。用0.5–1 mmol / L Ca ^2+处理可明显逆转F诱导的有害作用，但高剂量Ca ²⁺（2–8 mmol / L）可增强这些作用。综上所述，0.5-1 mmol / L Ca ²⁺可以通过内质网应激凋亡途径减轻F诱导的OB细胞损伤，为进一步研究Ca ²⁺治疗骨骼氟症提供了剂量依据。