Anti‐Inflammatory, Anti‐Colitis, and Antioxidant Effects of Salidroside against Dextran Sodium Sulfate Induced Ulcerative Colitis in Rats via Inhibition of NF‐κB‐INOS‐No and TLR4‐NF‐κB Signaling Pathways

ABSTRACT Ulcerative colitis is a persistent inflammatory bowel disorder that predominantly impacts the mucosal lining of the rectum and colon. Targeting inflammatory reactions serves a preventative function in the management of ulcerative colitis. Salidroside has already exhibited an anti‐inflammatory effect against various diseases. The current investigation demonstrated the protective effect of salidroside against dextran sodium sulfate (DSS)‐induced UC in rats. 3% DSS was dissolved in the drinking water and administered to the rats for induction of UC in rats and rats were orally administered the salidroside and sulfasalazine for 7 days. The body weight, macroscopic study, organ weight, water intake, food intake, antioxidant, apoptosis, cytokines and inflammatory parameters were estimated. The disease activity index was measured in all groups. The level of VCAM‐1, ICAM‐1, HO‐1 and Nrf2 were estimated. The mRNA expressions were estimated in the colon tissue. Histopathological study of the colon tissue was also performed. Salidroside treatment remarkably improved the body weight and altered the organ weight. Salidroside treatment significantly (p < 0.001) suppressed the DAI score along with alteration of oxidative stress (MDA, SOD, CAT, GSH), cytokines (TNF‐α, IL‐1, 1β, 6, 10, 18), inflammatory parameters (TGF‐β, PGE2, COX‐2, NF‐κB, iNOS), apoptosis (Bcl‐2, Bcl‐2:Bax ratio, Bax, caspase‐3) parameters. Salidroside treatment suppressed the level of VCAM‐1, NO, ICAM‐1, MPO and upgraded the level of Nrf2 and HO‐1. Salidroside treatment altered the mRNA expression of Ocln, ASC, TNF‐α, MCP‐1, ZO‐1, IFN‐γ, IL‐1β, IL‐6, iNOS, COX‐2, TGF‐β and TLR4. The results clearly demonstrated that salidroside may exert Anti‐inflammatory, anti‐colitis, and antioxidant effects by altering the expression of key genes involved in the NF‐κB‐iNOS‐NO and TLR4‐NF‐κB signaling pathways.