Displaying all 5 publications

  1. Tudave D, Radhakrishnan A, Chakravarthi S, Haleagrahara N
    Inflamm. Res., 2011 Oct;60(10):897-907.
    PMID: 21633874 DOI: 10.1007/s00011-011-0349-y
    OBJECTIVES: The study investigated the effect of collagen-induced arthritis in Dark Agouti (DA) rats on the level of C-reactive protein and inflammatory cytokine tumour necrosis factor-alpha (TNF-α).

    SUBJECTS: Female Dark Agouti (DA) rats.

    METHODS: Three different dosages of (2 mg/kg of body weight, 3 mg/kg of body weight and 4 mg/kg of body weight) collagen and complete Freund's adjuvant suspension were tested. After 45 days, serum C-reactive protein, TNF-α, superoxide dismutase and total glutathione assays were done. Radiographic and histopathological changes in the joints were compared.

    RESULTS: All three groups showed signs of arthritic changes, confirmed by histopathological and radiographic changes. Severe arthritic changes were seen in the rats injected with 4 mg/kg of body weight of collagen. There was a significant increase in C-reactive protein, TNF-α, super oxide dismutase and total glutathione levels in the plasma in arthritis rats and the changes were more significant with 4 mg/kg of collagen.

    CONCLUSION: These results demonstrated that the optimal dose to inject to experimental animals in order to get server arthritic changes was 4 mg/kg of collagen with complete Freund's adjuvant suspension. Severe arthritis changes induced significant elevation in plasma C-reactive protein and TNF-α levels.

  2. Harasstani OA, Moin S, Tham CL, Liew CY, Ismail N, Rajajendram R, et al.
    Inflamm. Res., 2010 Sep;59(9):711-21.
    PMID: 20221843 DOI: 10.1007/s00011-010-0182-8
    OBJECTIVES: We evaluated several flavonoid combinations for synergy in the inhibition of proinflammatory mediator synthesis in the RAW 264.7 cellular model of inflammation.

    METHODS: The inhibitory effect of chrysin, kaempferol, morin, silibinin, quercetin, diosmin and hesperidin upon nitric oxide (NO), prostaglandin E(2) (PGE(2)) and tumour necrosis factor-alpha (TNF-alpha) secretion from the LPS-induced RAW 264.7 monocytic macrophage was assessed and IC(50) values obtained. Flavonoids that showed reasonable inhibitory effects in at least two out of the three assays were combined in a series of fixed IC(50) ratios and reassessed for inhibition of NO, PGE(2) and TNF-alpha. Dose-response curves were generated and interactions were analysed using isobolographic analysis.

    RESULTS: The experiments showed that only chrysin, kaempferol, morin, and silibinin were potent enough to produce dose-response effects upon at least two out of the three mediators assayed. Combinations of these four flavonoids showed that several combinations afforded highly significant synergistic effects.

    CONCLUSIONS: Some flavonoids are synergistic in their anti-inflammatory effects when combined. In particular chrysin and kaempferol significantly synergised in their inhibitory effect upon NO, PGE(2) and TNF-alpha secretion. These findings open further avenues of research into combinatorial therapeutics of inflammatory-related diseases and the pharmacology of flavonoid synergy.

  3. Bhatia M, Landolfi C, Basta F, Bovi G, Ramnath RD, de Joannon AC, et al.
    Inflamm. Res., 2008 Oct;57(10):464-71.
    PMID: 18827968 DOI: 10.1007/s00011-008-7210-y
    Chemokines play a fundamental role in trafficking and activation of leukocytes in colonic inflammation. We investigated the ability of bindarit, an inhibitor of monocyte chemoattractant protein-1 (MCP-1/CCL2) synthesis, to inhibit chemokine production by human intestinal epithelial cells (HT-29) and its effect in trinitro-benzene sulfonic acid (TNBS)-induced colitis in mice.
  4. Tilwani RK, Vessillier S, Pingguan-Murphy B, Lee DA, Bader DL, Chowdhury TT
    Inflamm. Res., 2017 Jan;66(1):49-58.
    PMID: 27658702 DOI: 10.1007/s00011-016-0991-5
    OBJECTIVE AND DESIGN: Oxygen tension and biomechanical signals are factors that regulate inflammatory mechanisms in chondrocytes. We examined whether low oxygen tension influenced the cells response to TNFα and dynamic compression.

    MATERIALS AND METHODS: Chondrocyte/agarose constructs were treated with varying concentrations of TNFα (0.1-100 ng/ml) and cultured at 5 and 21 % oxygen tension for 48 h. In separate experiments, constructs were subjected to dynamic compression (15 %) and treated with TNFα (10 ng/ml) and/or L-NIO (1 mM) at 5 and 21 % oxygen tension using an ex vivo bioreactor for 48 h. Markers for catabolic activity (NO, PGE2) and tissue remodelling (GAG, MMPs) were quantified by biochemical assay. ADAMTS-5 and MMP-13 expression were examined by real-time qPCR. 2-way ANOVA and a post hoc Bonferroni-corrected t test were used to analyse data.

    RESULTS: TNFα dose-dependently increased NO, PGE2 and MMP activity (all p 

  5. Abdo AIK, Tye GJ
    Inflamm. Res., 2020 May;69(5):463-480.
    PMID: 32215665 DOI: 10.1007/s00011-020-01339-9
    PURPOSE: IL-23 is a central proinflammatory cytokine with a wide range of influence over immune response. It is implicated in several autoimmune diseases due to the infinite inflammatory loops it can create through the positive feedbacks of both IL-17 and IL-22 arms. This made IL-23 a key target of autoimmune disorders therapy, which indeed was proven to inhibit inflammation and ameliorate diseases. Current autoimmune treatments targeting IL-23 are either by preventing IL-23 ligation to its receptor (IL-23R) via antibodies or inhibiting IL-23 signaling by signaling downstream mediators' inhibitors, with each approach having its own pros and cons.

    METHODS: Literature review was done to further understand the biology of IL-23 and current therapies.

    RESULTS: In this review, we discuss the biological features of IL-23 and its role in the pathogenesis of autoimmune diseases including psoriasis, rheumatoid arthritis and inflammatory bowel diseases. Advantages, limitations and side effects of each concept will be reviewed, suggesting several advanced IL-23-based bio-techniques to generate new and possible future therapies to overcome current treatments problems.

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