Protective effects of anthocyanins on the nervous system injury caused by fluoride-induced endoplasmic reticulum stress in rats.

Long-term fluoride exposure can produce neurotoxicity. Anthocyanins, as antioxidants, have a certain protective effect in nerve damage. This study aimed to investigate the protective role of anthocyanins in fluoride-induced neurological damage due to endoplasmic reticulum stress (ERS). Using a fluoride-exposed Wistar rat model, we assessed learning memory capacity and pathologic and ultrastructural injury. The level of oxidative stress (OS) in vivo was detected by colorimetric method, the level of ERS was analyzed by immunohistochemistry, and the apoptosis of neuronal cells was observed by TUNEL staining. The results showed that fluoride exposure could decrease the learning and memory ability in rats, and led to histopathological and ultrastructural damage in the hippocampal CA1, CA3 and cortical regions. Fluoride exposure-induced OS in vivo, which further activates ERS, which was manifested by increased levels of ERS-related proteins GRP78, Caspase 12, and Caspase 3 in hippocampal CA1, CA3, and cortical regions, and eventually led to a significant increase in neuronal apoptosis rate. Notably, after anthocyanins treatment, pathological and ultrastructural damage was restored, the level of OS and ERS were significantly restored, and the apoptosis rate of neuronal cells was significantly reduced. In summary, as nutritional interventions, anthocyanins exert a protective role in fluoride-induced neurological injury.