Abstract
Excessive fluoride exposure can lead to health problems, such as fluorosis and neurotoxicity. However, effective therapeutic strategies for neurofluorosis remain elusive due to a limited understanding of the underlying molecular mechanisms. This study aimed to investigate the effects of Tanshinone IIA on spinal cord injury induced by high-fluoride exposure. To identify dysregulated genes associated with ferroptosis, we conducted an intersection analysis between differentially expressed genes in fluoride-treated HOS cells (GSE70719) and ferroptosis-related genes from the FerrDb database. A rat model of fluoride-induced spinal cord injury was established, revealing evidence of aberrant molecular and structural changes. Furthermore, the study demonstrated that Tanshinone IIA restored the altered expression of nine ferroptosis-related genes, eight fluorosis-related inflammatory indicators, and the observed structural changes. Overall, these findings suggest that Tanshinone IIA therapeutic potential in the treatment of fluoride-induced spinal cord injury by inhibiting ferroptosis and inflammation.