Eriodictyol attenuates TNBS-induced ulcerative colitis through repressing TLR4/NF-kB signaling pathway in rats.

Abstract

Ulcerative colitis (UC) is a chronic disease characterized by mucosal and submucosal inflammation, which has a low cure rate and is prone to relapse, due to the immune imbalance of the body. Inhibition of inflammation-related pathways can delay the progression of UC. Toll-like receptor 4 (TLR4) pathway is considered to be one of the important signaling pathways involved in colon inflammation. Eriodictyol (EDT) is a natural flavonoid widely distributed in foodborne plants. EDT plays an important role in the regulation of inflammation and related signaling pathways. However, whether EDT plays a role in UC remains unknown. Herein, we established a TNBS induced animal model of enteritis in Wistar rats. Our data confirmed the establishment of TNBS induced animal model of enteritis and the administration Eriodictyol in Wistar rats. EDT treatment alleviated TNBS-induced intestinal tissue injury in rats. We further found that EDT reduced MPO expression and regulated the cytokine parameters in TNBS-induced intestinal tissues of rats. The levels of TNF-α, IL-1β, IL-6, IL-10, IL-2, and IL-12 were also affected by the treatment of EDT. EDT also affected SOD, CAT, GSH-Px, and MDA level in rats with colitis. Moreover, EDT regulated TNBS-induced TLR4/NF-κB pathway activation, therefore inhibiting the progression of UC. Our results suggest that EDT could be a potential therapeutic agent for UC.