The Protective Effects of Herbacetin Against 2,4,6-Trinitrobenzene Sulfonic Acid-Induced Inflammatory Bowel Disease via Inhibition of the NF-κB Signaling Pathway

Abstract

The study investigated the effects of Herbacetin on inflammatory bowel disease (IBD) rats and Caco-2 cells with inflammatory injury induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS) and lipopolysaccharide (LPS), respectively. TNBS-induced IBD rats were administered with Mesalazine or Herbacetin, while LPS-induced Caco-2 cells were treated with various concentrations of Herbacetin. The body weight of rats was observed, and colon morphological characteristics were studied by H&E staining. The expressions of inflammatory cytokines in serum and T lymphocyte subsets in PB lymphocytes were analyzed. The results showed that Herbacetin treatment increased disease activity index, rats’ body weight, and survival rate in vivo. Moreover, Herbacetin was found to alleviate pathological injury and fibrosis in TNBS-induced rats. Flow cytometry analysis showed decreased percentages of CD3+ and CD8+ and an increased percentage of CD4+ after Herbacetin supplement. Furthermore, TNF-α and IL-1β were down-regulated, while IL-4 and IL-10 were up-regulated in Herbacetin treatment groups. Western blot analysis proved that Herbacetin suppressed the elevated ratio of p-p65/p65 and p-IκBα/IκBα induced by LPS. These findings suggest that Herbacetin can protect against TNBS-induced inflammatory response and immune injury by deactivating the NF-κB signaling pathway.