Evaluation of anti-arthritic potential of Trigonella foenum graecum L. (Fenugreek) mucilage against rheumatoid arthritis.

Rheumatoid arthritis is a chronic inflammatory joint disease characterized by synovial proliferation and tissue destruction. Pro-inflammatory cytokines like interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) play a key role in the disease process and elevate energy expenditure, which further increases the joint pain and stiffness. The present study was undertaken to explore the anti-arthritic potential of fenugreek mucilage in adjuvant induced arthritic rats. In the present study, paw volume was measured on the 7th, 14th and 21st day. Finally, animals were anaesthetized; blood samples and tissues were collected for the assay of inflammatory enzymes like cyclooxygenase, lipoxygenase; evaluated the level of cytokines like IL-6, TNF-α, arthritic index and rheumatoid factor. Fenugreek mucilage exhibited maximum percentage of edema inhibition at a dose of 75 mg/kg on 21st day of adjuvant arthritis. The effect was higher than that of standard drug, indomethacin. The activities of inflammatory enzymes and concentration of mediators were decreased on treatment with fenugreek mucilage. Cytology of synovial fluid showed mild inflammation with normal synoviocytes (mesothelial cells) tried to bring back to normal characteristics on supplementation with fenugreek mucilage. Based on the observations, it can be suggested that fenugreek mucilage possesses promising anti-arthritic property and it can be used as a therapeutic agent for arthritis.

Attenuation of atherosclerotic complications by modulating inflammatory responses in hypercholesterolemic rats with dietary Njavara rice bran oil.

Atherosclerosis is a chronic inflammatory disease. The role of inflammation in atherosclerosis is well established, with all stages of disease progression being assessed as inflammatory response to injury. Preventive treatments and drugs identified so far are based on lipid lowering strategies which also involves functional foods and dietary supplementation. The present study investigated the effect of supplementation of Njavara rice bran oil (NjRBO), extracted from a medicinal rice variety, to high cholesterol diet (HCD) fed rats on atherosclerosis by attenuating the inflammatory responses in PBMCs, aortic endothelial cells and macrophages. Adult male rats (Sprague-Dawley strain, weighing 100-120g) were grouped into 3 of six rats each. Group I served as control, Group II were fed high cholesterol diet (HCD) and Group III were fed a HCD and NjRBO (100mg/kg body weight). The experimental duration was 60days. Activities of cyclooxygenase, lipoxygenase, nitric oxide synthase, and myeloperoxidase, expression of Tumor necrosis factor-α, Interleukin-6, Interferon γ, monocyte chemoattractant protein-1, and cytosolic phospholipase A2 were found to be decreased on NjRBO supplementation which were increased in HCD fed rats. Expression of ICAM-1 and VCAM-1 in aortic endothelial cells was decreased significantly in NjRBO treatment than HCD fed rats. This attenuations were mainly due to inhibition in translocation of NF-κB into nucleus in aortic endothelial cells. Also, NjRBO treatment significantly decreased the gene expressions of TLR-2, TLR-4, and CD36 in both macrophages and endothelial cells than HCD fed rats indicates its anti-inflammatory effect via TLR - NF-κB signaling pathway. NjRBO has thereby shown to possess anti-atherogenic property by effectively modulating inflammatory mechanisms.

Tricin, flavonoid from Njavara reduces inflammatory responses in hPBMCs by modulating the p38MAPK and PI3K/Akt pathways and prevents inflammation associated endothelial dysfunction in HUVECs.

Previous studies revealed the potent anti-inflammatory activity of tricin, the active component of Njavara rice bran. Here, we report the involvement of specific signaling pathways in the protective effect of tricin against LPS induced inflammation in hPBMCs and the role of tricin in modulating endothelial dysfunction in LPS induced HUVECs. Pretreatment with tricin (15µM) significantly inhibited the release of TNF-α and was comparable to the specific pathway blockers like ERK inhibitor (PD98059), JNK inhibitor (SP600125) and p38 inhibitor (SB203580), whereas an increased release of TNF-α was observed in PI3K/Akt inhibitor (LY294002) treated cells. Tricin alone and combination treatment of tricin and SB203580 showed more significant inhibition of activation of COX-2 and TNF-α than that of SB203580 alone treated group. Combination treatment of tricin and LY294002 showed increased activation of COX-2 and TNF-α, proved that PI3K activation is essential for the anti-inflammatory effect of tricin. Studies conducted on HUVECs revealed the protective effect of tricin against endothelial dysfunction associated with LPS induced inflammation by inhibiting the activation of proinflammatory mediators like TNF-α, IFN-γ, MCP 1 by modulating NF-κB and MAPK signaling pathways. ELISA and flow cytometric analysis again confirmed the protection of tricin against endothelial damage, especially from the decreased activation of cell adhesion molecules like ICAM-1, VCAM-1 and E-Selectin upon tricin treatment. This work establishes the mechanism behind the potent anti-inflammatory activity of the flavonoid tricin.