In this study, p-coumaric acid was evaluated for its immunomodulatory and anti-inflammatory properties in vivo. The immunomodulatory effect of p-coumaric acid (100 mg/kg body weight) was assessed by evaluating its effect on cell-mediated immune responses (delayed type hypersensitivity reaction), serum immunoglobulin levels, and macrophage phagocytic index in rats. The anti-inflammatory effects of p-coumaric acid (100 mg/kg body weight) were investigated by examining its effect on expression of tumor necrosis factor (TNF-α) in synovial tissue by immunofluorescence confocal microscopy and circulating immune complexes in serum of adjuvant-induced arthritic rats. The increased cell-mediated immune responses and macrophage phagocytic index observed in control rats were significantly reduced (p < 0.05) upon treatment with p-coumaric acid implying its immunosuppressive property, whereas serum immunoglobulin levels were found to be increased in p-coumaric acid treated control rats. p-coumaric acid also showed significant (p < 0.05) anti-inflammatory effects in adjuvant-induced arthritic rats by effecting a decrease in the expression of inflammatory mediator TNF-α and circulating immune complexes. Indomethacin was used as a reference drug for anti-inflammatory studies. Thus, our results show that p-coumaric acid could be considered a potential immunosuppressive agent in treating autoimmune inflammatory diseases like rheumatoid arthritis.

The results of this study reveal the potential anti-inflammatory effect of p-Coumaric acid against monosodium urate crystal-induced inflammation in rats.

This study was designed to explore the underlying mechanism of p‐coumaric acid (CA), a dietary polyphenol in adjuvant‐induced arthritis (AIA) rat model with reference to synovitis and osteoclastogenesis. Celecoxib (COX‐2 selective inhibitor) (5 mg/kg b.wt) was used as a reference drug. CA remarkably suppressed the paw edema, body weight loss and inflammatory cytokine and chemokine levels (TNF‐α, IL‐1β, IL‐6, and MCP‐1) in serum and ankle joint of arthritic rats. Consistently, CA reduced the expression of osteoclastogenic factors (RANKL and TRAP), pro‐inflammatory cytokines (TNF‐α, IL‐1β, IL‐6, and IL‐17), and inflammatory enzymes (iNOS and COX‐2) in arthritic rats. However, OPG expression was found elevated. Besides, the abundance of transcription factors (NF‐κB‐p65, and p‐NF‐κB‐p65, NFATc‐1, and c‐Fos) and MAP kinases (JNK, p‐JNK, and ERK1/2) expression was alleviated in CA administered arthritic rats. In addition, CA truncated osteoclastogenesis by regulating the RANKL/OPG imbalance in arthritic rats and suppressing the RANKL‐induced NFATc‐1 and c‐Fos expression in vitro. Radiological (CT and DEXA scan) and histological assessments authenticated that CA inhibited TRAP, bone destruction and cartilage degradation in association with enhanced bone mineral density. Taken together, our findings suggest that CA demonstrated promising anti‐arthritic effect and could prove useful as an alternative drug in RA therapeutics. © 2017 BioFactors, 43(5):698–717, 2017

The present study was undertaken to investigate the anti-inflammatory effect of piperine against adjuvant-induced arthritis in rats, an experimental model for rheumatoid arthritis and compared it with that of the non-steroidal anti-inflammatory drug indomethacin. Administration of heat-killed Mycobacterium tuberculosis (0. 1 ml) intradermally into the right hind paw of rats resulted in increased paw volume, lysosomal enzymes, glycoproteins and tissue marker enzymes and decreased body weight. However, these changes were reverted to near normal levels upon piperine (30 mg/kg body weight, i.p.) treatment. Histopathological analysis of joints also revealed that synovial hyperplasia and mononuclear infiltration observed in arthritic rats were alleviated by piperine. Thus, the present study clearly indicated that piperine possesses promising anti-inflammatory effect against adjuvant-induced arthritis by suppressing inflammation and cartilage destruction.

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