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作 者:郑志[1,2] 姜林娟 朱瑜 朴丙熙 權英珠 ZHENG Zhi;JIANG Lin-juan;ZHU Yu;PARK Byounghee;KWON Youngjoo(School of Public Health,Xinxiang Medical University,Xinxiang 453000,China;Hanling Medical TechnologyResearch Institute Co.,Ltd.,Nanjing 211100,China;Raphagen Company,Seoul 04393,Republic of Korea;School of Pharmacy,Ewha Womans University,Seoul 04393,Republic of Korea)
机构地区:[1]新乡医学院公共卫生学院,河南新乡453000 [2]韩陵医药研究院有限公司,江苏南京211100 [3]莱帕坚(株)公司,韩国首尔04393 [4]梨花女子大学药学院,韩国首尔04393
出 处:《食品与药品》2022年第4期295-300,共6页Food and Drug
基 金:河南省自然科学基金项目(编号:162300410221);河南省引进国外智力专项(编号:HNGD2022066);新乡医学院海外归国博士启动金(编号:505098)。
摘 要:目的探讨鞣花酸对溃疡性结肠炎的改善效果及对COX2/p38/JNK/ERK/IκB-α/NF-κB和iNOS/3-NT/CYP2E1信号通路的影响。方法将30只BALB/c小鼠随机分为正常组、模型组、鞣花酸组,采用5%硫酸葡聚糖钠(DSS)诱导溃疡性肠炎模型,给药7 d后,观察小鼠结肠和肝组织形态学改变,酶联免疫吸附法(ELISA)和蛋白质印迹法(Western blot)检测小鼠血液、结肠组织炎症和氧化因子表达水平变化。结果与模型组比较,鞣花酸组小鼠的结肠长度、结肠重量、肝脏重量呈现改善(P<0.05)。与模型组比较,鞣花酸组小鼠的结肠上皮细胞完整,隐窝、环状细胞损伤、水肿程度较轻;肝组织未发现损伤,其表现与正常组一致。此外,与模型组比较,鞣花酸组的TNF-α、IL-1β、NO、COX2、p-p38、p-JNK、p-ERK、p-IκB-α、p-NF-κB、iNOS、3-NT、CYP2E1蛋白表达量降低(P<0.05)。结论鞣花酸可能通过抑制COX2/p38/JNK/ERK/IκB-α/NF-κB及iNOS/3-NT/CYP2E1信号通路,降低血液TNF-α、IL-1β、NO表达,对溃疡结肠炎的结肠和肝组织发挥改善功效。Objective To investigate the ameliorating effect of ellagic acid on ulcerative colitis in mice and its effect on COX2/p38/JNK/ERK/IκB-α/NF-κB and iNOS/3-NT/CYP2E1 signal pathways.Methods 30 BALB/c mice were randomly divided into normal group,UC model and positive(ellagic acid)group.The ulcerative enteritis model was induced by 5%dextran sulfate sodium(DSS).After 7 days of administration(5%DSS),the morphological and histopathological changes of colon and liver were observed,and the levels of inflammation and oxidative factors in blood and colon were detected by ELISA and Western blot.Results Compared with the model group,the colon length,colon weight and liver weight of mice in ellagic acid group showed improvement(P<0.05);the colonic epithelial cells in ellagic acid group were intact,and the damage and edema of crypt and annular cells were mild;no injury was found in the liver tissue,and its manifestation was consistent with that of the normal group.Compared with the UC model group,the levels of TNF-α,IL-1β,NO,COX2,p-p38,p-JNK,p-ERK,p-IκB-α,p-NF-κB,iNOS,3-NT and CYP2E1 in the positive(ellagic acid)group significantly decreased(P<0.05).Conclusion Ellagic acid may inhibit COX2/p38/JNK/ERK/IκB-α/NF-κB and iNOS/3-NT/CYP2E1 signaling pathways,thus reduce the expression of TNF-α,IL-1βand NO in blood,and improve the colon and liver tissue of ulcerative colitis.
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