Abstract

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 β-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 β-caryophyllene on gout. Certain methods including enzyme-linked immunosorbent assay, western blotting, and immunohistochemical staining were adopted to quantify. β-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-1β in the synovial tissue so as to reduce inflammation and protect ankle joints’ function. A new research approach in which β-caryophyllene treatment to acute attacks of gout is provided through the research results.

Highlights

  • Gout is regarded as an inflammatory reaction initiated by the deposition of monosodium urate (MSU) crystals around the joints

  • MSU-induced ones significantly swelled around the ankle joint, and the degree of swelling had spread to the limbs outside the joint. (Figure 1A); Compared with the normal control group, it is demonstrated in histological analysis that lymphocytes infiltration in joint synovial tissue (Figure 1B) could be found in the gout group

  • This study investigates the effects of β-Caryophyllene Ameliorates MSU-Induced Gouty β-caryophyllene on MSU-induced acute arthritis of inflammation

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Summary

Introduction

Gout is regarded as an inflammatory reaction initiated by the deposition of monosodium urate (MSU) crystals around the joints. The prevalence rate of men is higher than women (Jhang et al, 2018). As for the development of gout, the inflammatory response ranks first. The intrinsic mechanism should be summarized as that MSU crystals induce intra-articular inflammation through activating the complement system and recruiting neutrophils and macrophages. It gives rise to cartilage and synovial tissue damage, and it may eventually develop into joint damage and deformity (Kuo et al, 2015)

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