Effects of NaF on IL-1β gene expression depending on concentrations

Dede S., Usta A., Yüksek V., Çetin S.

XXXVTH Conference of the International Society for Fluoride Research (35.ISFR-2022), Harbin, China, 28 - 31 July 2022, vol.1, no.1, pp.61-62

  • Publication Type: Conference Paper / Summary Text
  • Volume: 1
  • City: Harbin
  • Country: China
  • Page Numbers: pp.61-62
  • Van Yüzüncü Yıl University Affiliated: Yes


ABSTRACT: Background/objectives. Fluoride is a highly reactive element that is excreted through the kidneys and metabolized in the liver. Prolonged and excessive fluoride intake leads to a disease known as fluorosis. Cell structures of liver and kidney tissues are damaged in fluorosis. IL-1B is a pro-inflammatory cytokine that plays a rolein pain, inflammation, and autoimmune conditions. Studies are carried out on the molecular metabolism of fluoride in our laboratory. This study was carried out to investigate the effects of fluoride on IL-1B in vitro and thus elucidate its potential role in cell proliferation and inflammation. Methods. NaF was used as fluoride source in this study. NaF concentrations were determined by MTT assay. NaF concentrations were determined as proliferative concentration (10 µM) and cytotoxic concentrations (IC25 (2250 µM) and IC50 (4250 µM)) at 24 hours. The determined NaF concentrations were administered to the cells. The IL-1B gene was considered the target gene. Total mRNA was isolated. mRNAs were converted to cDNA. The expression level of the target gene was determined by RT-qPCR method. Results. It was determined that it was expressed approximately 2.5 times in proliferative concentration, 3.4 times in IC25 concentration and 40 times in IC50 concentration. Conclusion. In conclusion, it was thought that NaF had a limited effect on IL-1B at proliferative and IC25 doses on kidney cells. At the same time, the IC50 was highly effective at toxic doses and can therefore be considered an indicator of damage. High expression of IL-1B gene in toxic concentration can be considered as an indicator of the importance of the inflammation pathway in the pathogenesis of fluoride-induced cell damage in the NRK-52E kidney cell