Astragaloside II alleviates the symptoms of experimental ulcerative colitis in vitro and in vivo

Background: Ulcerative colitis (UC) is a chronic inflammatory intestinal disease, and its morbidity is rising worldwide. Previous study indicated that astragaloside II (AS II), a monomeric compound, was used to treat bowel disease. However, the effects of AS II on UC remains unclear. Thus, this study aimed to investigate the therapeutic effects of AS II on experimental UC in vitro and in vivo.

Methods: CCD-18Co cells were stimulated by 1 μg/mL LPS to mimic UC in vitro. In addition, dextran sulfate sodium (DSS)-induced UC mouse model was established in vivo. CCK-8 assay was used to detect cell proliferation in vitro. Moreover, the concentrations of inflammatory factors interleukin 6 (IL-6), tumor necrosis factor-α (TNF-α), interleukin 1β (IL-1β), nitric oxide (NO), superoxide dismutase (SOD) and malondialdehyde (MDA) in CCD-18Co cells and colon tissues were determined by ELISA, respectively. Meanwhile, the expressions of hypoxia-inducible factor 1α (HIF-α), phospho-inhibitor of NF-κB (p-IκB) and phospho-NF-κB p65 (p-p65) were detected by western blotting in vitro and in vivo, respectively.

Results: In this study, the levels of pro-inflammatory cytokines TNF-α, IL-1β and IL-6 were significantly increased in lipopolysaccharide (LPS)-stimulated CCD-18Co cells. However, LPS-induced inflammatory response was markedly alleviated by AS II. In addition, LPS-induced HIF-α, p-IκB and p-p65 proteins increases were markedly ameliorated by AS II treatment. Moreover, AS II reduced disease activity index (DAI) scores and increased the colon lengths in DSS-treated mice. Meanwhile, AS II decreased the levels of IL-6, TNF-α, IL-1β, NO, MPO and MDA, and increased the level of SOD in colon of DSS-treated mice. Furthermore, AS II downregulated the expressions of HIF-α, p-IκB and p-p65 in DSS-induced UC in mice.

Conclusion: Our findings indicated that AS II could alleviate inflammatory response in LPS-induced CCD-18Co cells and in DSS-induced UC in mice. In conclusion, AS II may serve as a potential agent for the treatment of UC.