Abstract

Objectives In China, Oldenlandia diffusa (OD) is a natural herb that is widely used and has been proven to be effective in the treatment of rheumatoid arthritis (RA). This study aimed to preliminarily reveal the mechanism by which OD exerts its beneficial effect. Methods Ultra-performance liquid chromatography photodiode array was applied to identify the absorbable compounds in the plasma of collagen-induced arthritis (CIA) model rats. After 2 weeks, an OD decoction or the identified absorbable compound was administered to CIA rats. Morphology, X-ray images of the joints, pathological images, arthritis index, and cytokine (TNF-α and IL-6) levels were evaluated. Results p-Coumaric acid (p-CA) was identified as the absorbed compound in plasma. After administration of p-CA solution or the OD decoction, symptoms in the treated rats were alleviated as compared to the untreated model rats, and inflammatory cell infiltration was suppressed. The arthritis index and serum levels of TNF-α and IL-6 were decreased as compared to the control group. Conclusions OD may exert its anti-inflammatory effect on RA via its active ingredient, p-CA. This information sheds light on the mechanism by which OD exerts its anti-inflammatory effort in RA and forms the basis for further development of therapeutic agents for RA.

Highlights

  • Rheumatoid arthritis (RA) is a heterogeneous systemic autoimmune disease that impairs the quality of life of patients [1] and presents with different symptoms [2]

  • Recent studies have shown that TNF-α governs the crosstalk between fibroblast-like synoviocytes and chondrocytes [12] and might regulate the expressional changes in matrix-degrading enzymes and inflammatory mediators in fibroblast-like synoviocytes [12] and induce the inflammatory responses

  • We showed that the serum levels of TNF-α and IL-6 increased markedly in the collagen-induced arthritis (CIA) rat model of RA, and after treatment with p-Coumaric acid (p-CA) or Oldenlandia diffusa (OD) these cytokine levels decreased (Figure 7)

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Summary

Introduction

Rheumatoid arthritis (RA) is a heterogeneous systemic autoimmune disease that impairs the quality of life of patients [1] and presents with different symptoms [2]. Exterior changes involve joint malformation, swelling, and joint dysfunction [3, 4], while interior pathological changes mainly involve synovial hyperplasia and cartilage destruction. All of these changes are accompanied by systemic inflammatory responses [5, 6], involving many cytokines, such as TNF-α [7, 8] and IL-6 [9,10,11], which are responsible for initiating, propagating, and maintaining inflammation [12] in a complex network [13]. TNF-α governs the crosstalk between fibroblast-like synoviocytes and chondrocytes [12] and induce inflammatory responses. It is clear that inflammation plays an important role in the pathology of RA

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