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作 者:苏宇[1] 刘宪斌[1] 张翔宇 SU Yu;LIU Xianbin;ZHANG Xiangyu(Department of General Surgery,Shenyang Ninth People's Hospital,Shenyang Liaoning 110024,China)
机构地区:[1]沈阳市第九人民医院普通外科,辽宁沈阳110024
出 处:《四川中医》2021年第1期35-38,共4页Journal of Sichuan of Traditional Chinese Medicine
基 金:辽宁省自然科学基金指导计划(编号:20170540829)。
摘 要:目的:探讨积雪草苷对溃疡性结肠炎(UC)大鼠的作用及机制研究。方法:38只SD大鼠随机分为四组:正常组、模型组、积雪草苷0.9g·kg^(-1)组和积雪草苷0.6g·kg^(-1)组。采用TNBS溶液灌肠法构建UC大鼠模型。HE染色观察结肠组织病理变化;酶联免疫吸附法检测血清白细胞介素-4(IL-4)、肿瘤坏死因子-α(TNF-α)、内毒素(ET)水平;蛋白质免疫印迹法检测结肠组织中Toll样受体4(TLR4)、核因子κB(NF-κB)和pNF-κB水平。结果:与正常组比较,模型组疾病活动指数(DAI)评分、IL-4、TNF-α、ET、TLR4和pNF-κB水平均升高,差异均有统计学意义(P<0.05)。与模型组比较,积雪草苷组DAI评分、IL-4、TNF-α、ET、TLR4和pNF-κB水平均降低,积雪草苷0.9g·kg^(-1)组DAI评分、IL-4、TNF-α、ET、TLR4和pNF-κB水平均低于积雪草苷0.6g·kg^(-1)组,差异均有统计学意义(P<0.05)。结论:积雪草苷可降低UC大鼠炎症状态,保护结肠黏膜组织,其机制可能与调控TLR4/NF-κB通路表达有关。Objective: To explore the effect and mechanism of Asiaticoside for ulcerative colitis(UC) rats. Methods: 38 SD rats were randomly divided into four groups: normal group, model group, Asiaticoside 0.9 g·kg^(-1) group and Asiaticoside 0.6 g·kg^(-1) group. UC rat model was established by TNBS solution enema method. HE staining was used to observe the pathological changes of colonic tissues. Enzyme-linked immunosorbent assay was used to detect serum interleukin-4(IL-4),tumor necrosis factor-α(TNF-α),and endotoxin(ET) levels. Western blot was used to detect Toll-like receptor 4(TLR4),nuclear factor kappa B(NF-κB) and pNF-κB levels in colon tissues. Results: Compared with the normal group, the disease activity index(DAI) scores, IL-4,TNF-α,ET,TLR4 and pNF-κB levels in the model group were increased, and the differences were statistically significant(P<0.05). Compared with the model group, the DAI score, IL-4,TNF-α,ET,TLR4,and pNF-κB levels of the asiaticoside group decreased, and the levels of DAI score, IL-4,TNF-α,ET,TLR4,and pNF-κB in the asiaticoside 0.9 g·kg^(-1) group were lower than those in the asiaticoside 0.6 g·kg^(-1) group, and the differences were statistically significant(P<0.05). Conclusion: Asiaticoside can reduce the inflammatory status and protect the colonic mucosa in UC rats. The mechanism may be related to the regulation of TLR4/NF-κB pathway expression.
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