Abstract
Ulcerative colitis (UC) is a common chronic, idiopathic inflammatory bowel disease associated with inflammatory perturbation and oxidative stress. Umbelliferone (UMB) is a potent anti-inflammatory and antioxidant coumarin derivative. Depending on the possible mechanisms, we aimed to explore and elucidate the therapeutic potential of UMB on UC-inflammatory response and oxidative injury-induced via intrarectal administration of acetic acid (AA). Rats were assigned into four groups: control group, UMB (30 mg/kg) treated group, colitis model group (2 ml of AA; 3% v/v), and colitis treated with UMB groups. Our results exhibited that UMB improved macroscopic and histological tissue injury caused by the AA. Mechanistically, UMB reduced the elevated TNF-α, IL-6, MPO and VCAM-1 via effective downregulation of TLR-4, NF-κB and iNOS signaling pathway, thereby mediated potent anti-inflammatory effects. Moreover, UMB administration resulted in effective up-regulation of both PPARγ and SIRT1 signaling pathways, thereby inhibited both oxidative injury and inflammatory response. Conclusively, UMB protected against AA-induced UC in rats through suppressing of the TLR4/NF-κB-p65/iNOS signaling pathway and promoting the PPARγ/SIRT1 signaling. Indeed, our data proved the effectiveness of UMB in UC and introduced it as a potential therapeutic beneficial applicant for clinical application.
Acetic Acid-Producing Endophyte Lysinibacillus fusiformis Orchestrates Jasmonic Acid Signaling and Contributes to Repression of Cadmium Uptake in Tomato Plants
