oroxylin-a-7-o-glucuronide and Disease-Models--Animal

oroxylin-a-7-o-glucuronide has been researched along with Disease-Models--Animal* in 1 studies

Other Studies

1 other study(ies) available for oroxylin-a-7-o-glucuronide and Disease-Models--Animal

Article	Year
Oroxyloside prevents dextran sulfate sodium-induced experimental colitis in mice by inhibiting NF-κB pathway through PPARγ activation. Biochemical pharmacology, 2016, Apr-15, Volume: 106 Oroxyloside, as a metabolite of oroxylin A, may harbor various beneficial bioactivities which have rarely been reported in the previous studies. Here we established the dextran sulfate sodium (DSS)-induced experimental colitis and evaluated the anti-inflammatory effect of oroxyloside in vivo. As a result, oroxyloside attenuated DSS-induced body weight loss, colon length shortening and colonic pathological damage. Furthermore, oroxyloside inhibited inflammatory cell infiltration and decreased myeloperoxidase (MPO) and inducible nitric oxide synthase (iNOS) activities as well. The production of pro-inflammatory cytokines in serum and colon was also significantly reduced by oroxyloside. We unraveled the underlying mechanisms that oroxyloside inhibited NF-κB pathway by activating Peroxisome Proliferator-Activated Receptor γ (PPARγ) to attenuate DSS-induced colitis. Moreover, we investigated the anti-inflammatory effect and mechanisms of oroxyloside in the mouse macrophage cell line RAW264.7 and bone marrow derived macrophages (BMDM). Oroxyloside decreased several LPS-induced inflammatory cytokines, including IL-1β, IL-6 and TNF-α in RAW264.7 and BMDM. We also found that oroxyloside inhibited LPS-induced activation of NF-κB signaling pathway via activating PPARγ in RAW 264.7 and BMDM. Docking study showed that oroxyloside could bind with PPARγ. GW9662, the inhibitor of PPARγ, and PPARγ siRNA transfection blocked the effect of oroxyloside on PPARγ activation. Our study suggested that oroxyloside prevented DSS-induced colitis by inhibiting NF-κB pathway through PPARγ activation. Therefore, oroxyloside may be a promising and effective agent for inflammatory bowel disease (IBD). Topics: Anilides; Animals; Anti-Inflammatory Agents, Non-Steroidal; Cell Line; Colitis; Dextran Sulfate; Disease Models, Animal; Female; Flavones; Gene Expression Regulation; Glucuronides; Interleukin-1beta; Interleukin-6; Macrophages; Mice; Mice, Inbred C57BL; Molecular Docking Simulation; NF-kappa B; Nitric Oxide Synthase Type II; Peroxidase; PPAR gamma; RNA, Small Interfering; Signal Transduction; Tumor Necrosis Factor-alpha	2016

Article

Year

Oroxyloside prevents dextran sulfate sodium-induced experimental colitis in mice by inhibiting NF-κB pathway through PPARγ activation.

Biochemical pharmacology, 2016, Apr-15, Volume: 106

Oroxyloside, as a metabolite of oroxylin A, may harbor various beneficial bioactivities which have rarely been reported in the previous studies. Here we established the dextran sulfate sodium (DSS)-induced experimental colitis and evaluated the anti-inflammatory effect of oroxyloside in vivo. As a result, oroxyloside attenuated DSS-induced body weight loss, colon length shortening and colonic pathological damage. Furthermore, oroxyloside inhibited inflammatory cell infiltration and decreased myeloperoxidase (MPO) and inducible nitric oxide synthase (iNOS) activities as well. The production of pro-inflammatory cytokines in serum and colon was also significantly reduced by oroxyloside. We unraveled the underlying mechanisms that oroxyloside inhibited NF-κB pathway by activating Peroxisome Proliferator-Activated Receptor γ (PPARγ) to attenuate DSS-induced colitis. Moreover, we investigated the anti-inflammatory effect and mechanisms of oroxyloside in the mouse macrophage cell line RAW264.7 and bone marrow derived macrophages (BMDM). Oroxyloside decreased several LPS-induced inflammatory cytokines, including IL-1β, IL-6 and TNF-α in RAW264.7 and BMDM. We also found that oroxyloside inhibited LPS-induced activation of NF-κB signaling pathway via activating PPARγ in RAW 264.7 and BMDM. Docking study showed that oroxyloside could bind with PPARγ. GW9662, the inhibitor of PPARγ, and PPARγ siRNA transfection blocked the effect of oroxyloside on PPARγ activation. Our study suggested that oroxyloside prevented DSS-induced colitis by inhibiting NF-κB pathway through PPARγ activation. Therefore, oroxyloside may be a promising and effective agent for inflammatory bowel disease (IBD).

Topics: Anilides; Animals; Anti-Inflammatory Agents, Non-Steroidal; Cell Line; Colitis; Dextran Sulfate; Disease Models, Animal; Female; Flavones; Gene Expression Regulation; Glucuronides; Interleukin-1beta; Interleukin-6; Macrophages; Mice; Mice, Inbred C57BL; Molecular Docking Simulation; NF-kappa B; Nitric Oxide Synthase Type II; Peroxidase; PPAR gamma; RNA, Small Interfering; Signal Transduction; Tumor Necrosis Factor-alpha

2016