Introduction This research aims to investigate the mechanism of action of Lactobacillus rhamnosus AFY02 (LR-AFY02) in mice with acute gouty arthritis. Using sodium urate, we created a mouse model of acute gouty arthritis.
Methods We then examined the degree of foot swelling, pain threshold, blood biochemical indicators, histopathological changes, and mRNA expression changes to determine the effectiveness and mechanism of LR-AFY02 in preventing acute gouty arthritis in mice.
Results The outcomes of the animal experiment demonstrated that LR-AFY02 can decrease the severity of mouse foot edema and raise pain threshold. In the ankle joint tissues of mice with acute arthritis, LR-AFY02 can increase the enzyme activity of superoxide dismutase (SOD) and the level of glutathione (GSH), while lowering the enzyme activity of myeloperoxidase (MPO) and the level of malondialdehyde (MDA). Interleukin-6 (IL-6), IL-10, IL-1β, and tumor necrosis factor-alpha (TNF-α) levels in the blood of mice with acute arthritis are also decreased by LR-AFY02. Histopathological findings demonstrated that LR-AFY02 reduced tissue damage in the mouse foot and ankle joints. The findings of the qPCR experiment showed that LR-AFY02 may suppress the mRNA expression of extracellular signal-regulated kinase 1/2 (ERK1/2), cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), IL-6, interferon gamma (IFN-γ), and TNF- in the tissues of the ankle joints of mice with acute arthritis. Additionally, LR-AFY02 has the ability to increase the expression of catalase (CAT), manganese superoxide dismutase (Mn-SOD), and copper/zinc superoxide dismutase (Cu/Zn-SOD).
Conclusion As a result, it is clear that Lactobacillus rhamnosus AFY02 is more effective than glucosamine sulfate at preventing acute gouty arthritis. It is a strain with potential as a probiotic.