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作 者:詹原泉 丛龙玲 吕永慧 黄雅静 谢英杰 周婉妃 吴宇金 ZHAN Yuanquan;CONG Longling;LYU Yonghui;HUANG Yajing;XIE Yingjie;ZHOU Wanfei;WU Yujin(Department of Spleen and Stomach Disease,The Affiliated TCM Hospital of Guangzhou Medical University,Guangzhou 510130,China;Guangdong Provincial People's Hospital,Guangzhou 510000,China;Guangzhou University of Chinese Medicine,Guangzhou 510405,China)
机构地区:[1]广州医科大学附属中医医院脾胃科,广州510130 [2]广东省人民医院,广州510000 [3]广州中医药大学,广州510405
出 处:《世界中医药》2022年第14期1990-1994,2001,共6页World Chinese Medicine
基 金:广东省中医药局基金项目(20181199,20173029);广州市医药卫生科技项目(20182A011013)。
摘 要:目的:观察肠炎清对溃疡性结肠炎(UC)大鼠的保护作用及对TGF-β_(1)/Smad3/ERK信号通路的调控作用。方法:将25只雌性SD大鼠随机分为5组:空白对照组、模型组、美沙拉嗪组、肠炎清低剂量组和肠炎清高剂量组,除空白对照组外,其余大鼠均采用2,4,6三硝基苯磺酸(TNBS)诱导,建立UC模型。造模24 h后,模型组、空白对照组分别用0.9%生理盐水灌胃;美沙拉嗪对照组以30 mg/kg艾迪莎混悬液灌胃;肠炎清高剂量组以147.2 g/kg肠炎清灌胃;肠炎清低剂量组以36.8 g/kg肠炎清灌胃;1次/d,时间固定,持续7 d。检测结肠黏膜组织中转化生长因子(TGF)-β_(1)、Smad3、胞外信号调节激酶(ERK)磷酸化的水平及TGF-β_(1)信号通路活化的程度。结果:模型组ERK表达水平最低,低于溶媒对照组、美沙拉嗪组、肠炎清高剂量组和低剂量组,肠炎清剂量组该指标水平随剂量升高而上升,且高剂量肠炎清组ERK表达水平显著高于模型组。模型组TGF-β_(1)和Smad3高于美沙拉嗪组组、空白对照组和肠炎清低剂量组及高剂量组。结论:肠炎清对UC大鼠肠黏膜具有保护作用,其机制可能与通过下调TGF-β_(1)-Smad3通路,提高ERK表达有关。Objective:To observe the protective effect of Changyanqing on rats with ulcerative colitis and its regulation of transforming growth factor-β_(1)(TGF-β_(1))/mothers against decapentaplegic homolog 3(Smad3)/extracellular signal-regulated kinases(ERK)signaling pathway.Methods:A total of 25 female SD rats were randomly divided into 5 groups:blank control group,model group,mesalazine group,Changyanqing low-dose group and Changyanqing high-dose group.Except for the blank control group,the rest rats were injected with 2,4,6-Trinitrobenzenesulfonic acid(TNBS)to establish a UC model.Then 24 h after modeling,the TNBS model group and the blank control group were given 0.9%normal saline by gavage;the mesalazine group was given 30 mg/kg mesalazine suspension by gavage;the Changyanqing high-and low-dose groups were intragastrically administered with 147.2 g/kg and 36.8 g/kg Changyanqing,respectively,at a fixed time once a day for 7 days.The phosphorylation level of TGF-β_(1),Smad3,and ERK and the activation degree of TGF-β_(1) signaling pathway in colonic mucosa were detected.Results:The ERK expression level in the model group was the lowest among all groups.The ERK expression level in Changyanqing high-and low-dose groups increased with the increase of the dose,and this index of Changyanqing high-dose group was significantly higher than that of the model group.The levels of TGF-β_(1) and Smad3 in the model group were the highest among all groups.Conclusion:Changyanqing had a protective effect on the intestinal mucosa of UC rats and played a role in intestinal repair,and its mechanism of action might be related to down-regulating the TGF-β_(1)/Smad3 pathway and increasing the expression of ERK.
关 键 词:肠炎清 大鼠 转化生长因子-β_(1) 信号传导蛋白-3 细胞外信号调节激酶 作用机制 溃疡性结肠炎 信号通路
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