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Abstract Background Berberine hydrochloride is one the effective compound among Rhizoma Coptidis, Cortex Phellodendri, and other plants. There are several clinical functions of berberine hydrochloride including anti-inflammation, antitumor and immunoregulatory. However, the anti-inflammatory of berberine hydrochloride in ulcerative colitis is barely understood. In this study, we aimed to explore the effects of berberine hydrochloride on dextran sulfate sodium (DSS)-induced rats model of ulcerative colitis. Methods The severity of colitis were measured by body weight, survial rate, colon length and disease activity index (DAI) score. The cytokines expression include IL-1, IL-1β, IL-4, IL-6, IL-10, IL-12, TNF-α, TGF-β and IFN-γ were performed by RT-PCR and ELISA. Signaling pathway proteins such as p-STAT3, STAT3, p-NF-κB p65 and NF-κB p65 were analyzed by western blot and immunofluorescence. The proteins expression of tight junction were explored using western blotting and immunohistochemistry. Result Rats were administered berberine hydrochloride showed less weight loss and longer colon length than the DSS-induced group. The expression of IL-1, IL-1β, IL-6, IL-12, TNF-α, TGF-β and IFN-γ were suppressed, yet the expression of IL-4 and IL-10 were up-regulated by berberine hydrochloride and sulphasalazine treatment compared to the model group. Meanwhile, treatment with berberine hydrochloride effectively increased the expression of SIgA and decreased the expression of iNOS, MPO, MDA. In terms of the biochemical analyses, the results showed that the expression of p-STAT3 was signifcantly increased, while the expression of p-NF-κB (p65) was suppressed compared to the model group via western blot and immunofluorescence analysis. Conclusions Berberine hydrochloride has beneficial effects in UC. The possible mechanism of anti-inflammatory response by berberine hydrochloride may involve in the blocking of the IL-6/STAT3/NF-κB signaling pathway. Collectively, these fndings provide evidence that berberine hydrochloride might be a useful herb medicine and serve as a promising novel therapy in the treatment of UC in humans. Highlights • Berberine hydrochloride has the anti-inflammatory effect in ulcerative colitis. • Berberine hydrochloride could suppress apoptosis in ulcerative colitis. • Berberine hydrochloride has protective effects on DSS-induced ulcerative colitis via IL-6/STAT3/NF-κB pathway in rats. [ABSTRACT FROM AUTHOR]

Abstract 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-1β-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-β and TNF-α 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-κB 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-κB pathway. Highlights • Gallic acid has the anti-inflammatory effect in ulcerative colitis; • Gallic acid efficiently suppressed NF-κB signaling pathway in TNBS-induced UC. • Gallic acid plays an anti-inflammatory role in UC via inhibiting NF-κB pathway. [ABSTRACT FROM AUTHOR]