β-Caryophyllene Ameliorates MSU-Induced Gouty Arthritis and Inflammation Through Inhibiting NLRP3 and NF-κB Signal Pathway: In Silico and In Vivo

Gouty arthritis serves as an acute reaction initiated by the deposition of monosodium urate (MSU) crystals around the joints. In this study, the anti-inflammatory effects of phytochemical beta-caryophyllene on MSU crystal-induced acute gouty arthritis in vivo and in silico were explored. Through bioinformatics methods and molecular docking, it screened the specific influence pathway of beta-caryophyllene on gout. Certain methods including enzyme-linked immunosorbent assay, western blotting, and immunohistochemical staining were adopted to quantify. beta-caryophyllene significantly reduced inflammation and function of ankle joints in MSU Crystals-induced gouty arthritis rats, while decreasing serum cytokine levels. Furthermore, it inhibited the expressions of NLRP3, Caspase-1, ASC, TLR4, MyD88, p65, and IL-1 beta in the synovial tissue so as to reduce inflammation and protect ankle joints' function. A new research approach in which beta-caryophyllene treatment to acute attacks of gout is provided through the research results.

Automated summary

The study explored the anti-inflammatory effects of beta-caryophyllene on MSU crystal-induced acute gouty arthritis. Beta-caryophyllene significantly reduced inflammation in the ankle joints and decreased serum cytokine levels in gouty arthritis rats. Furthermore, it inhibited the expressions of inflammatory markers in the synovial tissue.