【摘要】 目的观察白芷乙素对溃疡性结肠炎小鼠的作用。方法将60只雄性SPF级C57BL/6小鼠随机分为空白对照组、模型组、柳氮磺胺吡啶组(0.5 g/kg)、白芷乙素低、中、高3个剂量组(6、12、24 mg/kg)。溃疡性结肠炎小鼠模型通过自由饮用3%葡聚糖硫酸钠(DSS)溶液进行构建,造模当天灌胃给药,连续7 d。每天对各组小鼠的疾病活动指数(DAI)进行评分;小鼠结肠进行病理学观察(HE染色);酶联免疫检测法(ELISA)检测结肠组织TNF-α、IL-1β、IL-6和IL-10的水平以及化学发光法检测结肠组织SOD活性以及MDA含量;Western blot法检测TLR4和NF-κB p65蛋白的表达水平。结果与空白对照组比较,模型组DAI评分明显升高(P<0.01),结肠组织损伤严重,可见大量的炎症细胞浸润。结肠组织TNF-α、IL-1β和IL-6水平明显升高(P<0.01),IL-10水平明显降低(P<0.01),SOD活性显著降低(P<0.01),MDA水平明显升高(P<0.01)。结肠组织TLR4、NF-κB p65蛋白表达水平明显升高(P<0.01)。与模型组比较,白芷乙素和柳氮磺胺吡啶组以上指标均能明显改善,如降低DAI评分(P<0.05),减轻结肠组织损伤,减少结肠组织炎症细胞的浸润,降低结肠组织TNF-α、IL-1β和IL-6的水平(P<0.05),升高结肠组织IL-10水平(P<0.05),升高SOD活性(P<0.05),降低MDA水平(P<0.05),降低结肠组织TLR4和NF-κB p65蛋白表达水平(P<0.05)。结论白芷乙素对DSS诱导的溃疡性结肠炎小鼠具有一定的保护作用,其机制可能与抑制炎症、抗氧化损伤以及调节TLR/NF-κB信号通路有关。更多还原

【Abstract】 Objective To explore the effect of ammidin on mice with ulcerative colitis. Methods Sixty SPF C57 BL/6 male mice were randomly divided into the blank control group, the model group, sulfasalazine group(0.5 g/kg), and low, medium and high doses of ammidin groups(6, 12 and 24 mg/kg). The mouse model of ulcerative colitis was constructed by freely drinking 3% dextran sodium sulfate(DSS) solution. The drug was administered by gavage on the day of modeling for 7 days. The disease activity index(DAI) of each group was scored every day.The pathology of colon tissues was observed in mice(HE staining).The levels of TNF-α, IL-1β,IL-6 and IL-10 in colon tissues were detected by enzyme-linked immunoassay(ELISA). SOD activity and MDA content in colon tissues were detected by chemiluminescence assay. The expression of TLR4 and NF-κB p65 protein was detected by western blot.Results Compared with the blank control group, the DAI score of the model group was significantly increased(P<0.01), colon tissue was seriously damaged, and a large number of inflammatory cells were detected. The levels of TNF-α, IL-1β and IL-6 in colon tissue were significantly increased(P<0.01). In contrast, the level of IL-10 was significantly decreased(P<0.01), SOD activity was significantly reduced(P<0.01) and the MDA level was significantly increased(P<0.01). The protein expression levels of TLR4 and NF-κB p65 in colon tissues were significantly increased(P<0.01).Compared with the model group, the above indexes were significantly improved in the ammidin group and sulfasalazine groups, such as reducing DAI score(P<0.05), reducing colon tissue injury, reducing the infiltration of inflammatory cells in colon tissue, and decreasing the levels of TNF-α, IL-1β and IL-6 in colon tissue(P<0.05). Meantime, the levels of IL-10, SOD, MDA and TLR4 and NF-κB p65 in colon tissues were increased(P<0.05), and the levels of SOD and MDA were decreased(P<0.05). Conclusion Ammidinhas a protective effect on DSS-induced ulcerative colitis in mice, and its mechanism may be related to inhibiting inflammation, antioxidant damage and regulating TLR/NF-κB signaling pathway.更多还原