Strontium Attenuates LPS-Induced Inflammation via TLR4/MyD88/NF-κB Pathway in Bovine Ruminal Epithelial Cells

Subacute ruminal acidosis (SARA) is a common nutritional metabolic disease in ruminants that causes significant economic losses to dairy farming. Strontium (Sr) is known to be involved in bone metabolism and exhibits potent anti-inflammatory effects. To evaluate the effect of Sr on inflammation in bovine ruminal epithelial cells, a model of LPS-induced inflammation was established in this study, and the cell viability of bovine ruminal epithelial cells was measured using CCK-8. The production of pro-inflammatory cytokines was measured by ELISA and real-time PCR, respectively. The related proteins of the TLR4/MyD88/NF-kappa B pathway were assayed through Western blotting, and the fluorescence of p-p65 and p-I kappa B were assayed by immunofluorescence. Molecular docking of Sr and TLR4/MyD88/NF-kappa B pathway-related proteins was performed using MIB2 (http://bioinfo.cmu.edu.tw/MIB2/). Results showed that after treatment for 24 h, the cell viability was decreased at the high concentration of Sr (>= 10 mmol/L). Sr significantly decreased the production of TNF-alpha, IL-1 beta, and IL-6, downregulated the related proteins expression of the TLR4/MyD88/NF-kappa B pathway, and reduced the fluorescence levels of p-p65 and p-I kappa B. The NF-kappa B pathway inhibitor PDTC and molecular docking further revealed that Sr reduced LPS-induced pro-inflammatory cytokines production via the TLR4/MyD88/NF-kappa B pathway. These results suggest that Sr reduces LPS-induced pro-inflammatory cytokines production via the TLR4/MyD88/NF-kappa B pathway, thereby exerting an anti-inflammatory effect in bovine ruminal epithelial cells, providing a basis for Sr in the treatment of bovine rumen acidosis disease.