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Calcium relieves fluoride-induced bone damage through the PI3K/AKT pathway
Jinming Wang1, Huimiao Xu, Xiaofang Cheng
1College of Animal Science and Veterinary Medicine, Shanxi Agricultural University, Taigu 030801, Shanxi, PR China.
Calcium carbonate (CaCO3) supplementation mitigates sodium fluoride (NaF)-induced bone damage by regulating the phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT) signaling pathway. This study reveals a novel mechanism for alleviating bone fluorosis.
Area of Science:
- Biochemistry
- Toxicology
- Cell Biology
Background:
- Bone fluorosis, a condition caused by excessive fluoride intake, primarily affects bone health.
- While calcium (Ca) is known to alleviate bone fluorosis, the underlying molecular mechanisms, particularly involving the PI3K/AKT pathway, remain unclear.
Purpose of the Study:
- To investigate the role of calcium carbonate (CaCO3) in mitigating fluoride-induced bone damage.
- To elucidate the involvement of the phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT) signaling pathway in CaCO3's protective effects against fluorosis.
Main Methods:
- Rats were treated with sodium fluoride (NaF) and/or CaCO3 for 120 days.
- Histopathological examination of bone tissue was performed.
- Biochemical markers of bone metabolism and gene expression levels related to the PI3K/AKT pathway were analyzed using qRT-PCR and Western blotting.
Main Results:
- NaF treatment induced bone histopathological injury, altered bone metabolism markers (increased alkaline phosphatase and tartrate-resistant acid phosphatase, decreased serum Ca), and activated the PI3K/AKT pathway by modulating key gene expressions.
- CaCO3 supplementation reversed NaF-induced histopathological changes and normalized biochemical markers.
- CaCO3 alleviated the activation of the PI3K/AKT pathway by reversing the expression changes of its related genes.
Conclusions:
- CaCO3 supplementation effectively mitigates fluoride-induced bone damage in rats.
- The protective effect of CaCO3 is mediated through the regulation of the PI3K/AKT signaling pathway, highlighting a novel therapeutic mechanism for bone fluorosis.
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