The protective effect of syringic acid on dextran sulfate sodium-induced experimental colitis in BALB/c mice.

Inflammatory bowel diseases involve chronic intestinal inflammation which is mostly caused by Crohn's disease and ulcerative colitis (UC) conditions. Patients having UC are prone to colorectal cancer and dysplastic polyps, and also have sporadic adenomas. Syringic acid (SA) possesses many health benefits including antioxidant, anti-bacterial, and anti-cancer. This study was aimed to identify the effects of SA on UC, using a murine experimental model. Clinical symptoms and weight loss were significantly reduced in mice induced with dextran sulfate sodium (DSS) and treated with SA, compared to untreated mice. The effects of SA exhibited in DSS-induced mice were associated with significant decrease in the expressions levels of inflammatory mediators such as inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), pro-inflammatory cytokines (tumor necrosis factor [TNF-α], interleukin [IL-1β and IL-6]), remarkable amelioration of colonic architectural disruption, and a significant reduction in the activity of colonic myeloperoxidase. To further confirm the anti-inflammatory property of SA, RAW 264.7 cells were stimulated with lipopolysaccharides. SA dose-dependently inhibited the cytokines TNF-α, IL-1β, and IL-6. It also decreased the expressions of p65-NF-κB and IκB, thus reducing the activation and nuclear accumulation of p-STAT-3^Y705 . This prohibited the degradation of inhibitory protein, IκB, as well as inhibited the nuclear translocation of p65-NF-κB in colonic tissue. It was concluded that SA has a potential to limit inflammation via inhibiting the p65-NF-κB and STAT3 signaling; hence it can be used for therapeutic purposes.