Cuixia Qiao1, Jin'e Wan2, Lize Zhang1, Bo Luo3, Penglin Liu1, Aiting Di1, Hairui Gao1, Xiaomei Sun1, Gang Zhao1. 1. Department of Anorectal, The Affiliated Hospital of Qingdao University Qingdao 266003, Shandong, China. 2. Department of High Pressure Oxygen, The Affiliated Hospital of Qingdao University Qingdao 266003, Shandong, China. 3. Department of Urology, Songshan Hospital of Qingdao University Qingdao 266000, Shandong, China.
Abstract
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. AJTR
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 UCmouse 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. AJTR
Authors: Philip Alex; Nicholas C Zachos; Thuan Nguyen; Liberty Gonzales; Tian-E Chen; Laurie S Conklin; Michael Centola; Xuhang Li Journal: Inflamm Bowel Dis Date: 2009-03 Impact factor: 5.325
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