Gallic acid improved inflammation via NF-κB pathway in TNBS-induced ulcerative colitis

Gallic acid (GA), as an active component, has been found in many fruits and plants, and it exhibits potential protective effects, such as anti-inflammatory, antioxidant, antiviral and anticancer. However, the effects of GA on ulcerative colitis (UC) remain unknown. The purpose of this study was to investigate the effects of GA on IL-1 beta-induced HIEC-6 cells and TNBS-induced UC in mice. Various biochemical analyses including proliferation and apoptosis were assessed in HIEC-6 cells. In addition, body weight of mice, the level of cytokines and histological changes were utilized to analyze the GA protecting mice with UC. Our results showed that administration of GA significantly increased the expressions of IL-4, and IL-10, while down-regulated IL-1, IL-6, IL-12, IL-17, IL-23, TGF-beta and TNF-alpha expressions compared with a model control group in vitro and in vivo. Moreover, flow cytometry and TUNEL analysis revealed that administration of GA significantly inhibited the apoptosis of HIEC-6 cells and mics in UC. Furthermore, pretreatment with GA obviously reversed the decrease in body weight, increase in colon weight, and attenuated the histological changes derived from UC. In addition, western blot analysis demonstrated that GA efficiently suppressed NF-kappa B signaling pathway in TNBS-induced UC. In conclusion, the findings of this study demonstrated that GA plays an anti-inflammatory role in UC via inhibiting NF-kappa B pathway.