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作 者:施花锦[1] 王小娟[2] 郭建生[1] 伍参荣[1] 夏历[2] 刘羽[1]
机构地区:[1]湖南中医药大学,湖南长沙410007 [2]湖南中医药大学第一附属医院,湖南长沙410007
出 处:《世界中西医结合杂志》2011年第9期751-753,789,共4页World Journal of Integrated Traditional and Western Medicine
基 金:湖南省自然科学基金项目(No.06JJ4038);湖南省教育厅资助科研项目(No.07c496)
摘 要:目的探讨IκB分子的上游蛋白激酶(IKKβ)对幽门螺杆菌相关性胃炎(HAG)病理变化的可能机制及灭幽汤在治疗HAG时的影响效应。方法建立HAG模型,采用幽门螺杆菌(H.py-lori)菌液灌胃造模,将造模成功的小鼠按体重随机分为模型组、丽珠得乐组、灭幽汤组。采用免疫组化法检测胃黏膜组织中核转录因子(NF-κB)I、KKβ的蛋白表达情况。HE染色观察胃组织病理变化。结果灭幽汤组能明显减轻胃组织的炎症反应,能抑制HAG胃组织中NF-κBI、KKβ蛋白的活性。正常对照组小鼠胃黏膜组织细胞内均有少量IKKβ、NF-κB表达。与正常对照组比较,模型组小鼠胃黏膜IKKβ及NF-κB表达增加(P<0.05);与模型组比较,灭幽汤组小鼠胃黏膜IKKβ及NF-κB表达降低(P<0.05)。结论灭幽汤能抑制H.pylori,改善胃黏膜血流,减轻胃黏膜炎症。NF-κB和IKKβ在HAG的炎症反应中发挥重要的作用,灭幽汤治疗HAG的机制可能是通过抑制IKKβ的激活和阻止NF-κB的活化实现的。Objective To explore the potential mechanism of upstream protein kinasa(IKKβ)of IκB molecules on the pathological change of H.plyori gastritis(HAG)as well as the effect of meiyoutang on HAG.Methods The gastric infusion with H.pylori solution was used to set up HAG model.The successfully modeled mice were divided randomly into a model group,a bismuth potassium citrate tablet group and a mieyoutang group according to the body weight.The immunohistochemical assay was adopted to detect the protein expressions of nuclear transcription factor(NF-κB)and IKKβ.HE staining was provided to observe the pathological change of gastric tissue.Results Mieyoutang remarkably alleviated the inflammatory reaction of gastric tissue and inhibited the activities of NF-κB and IKKβ.There were few IKKβ and NF-κB expressions in gastric mucosal cells of mice in normal group.Compared with normal control group,the expressions of IKKβ and NF-κB in gastric mucosa of mice increased in model group(P0.05).Compared with model group,the expressions of IKKβ and NF-κB in gastric mucosa of mice decreased in mieyoutang group(P0.05).Conclusion Mieyoutang inhibits H.pylori,improves blood flow of gastric mucosa and alleviates gastric mucosal inflammation.NF-κB and IKKβ play the important role in inflammatory reaction of HAG.Mieyoutang treats HAG probably through its inhibition of IKKβ and NF-κB from activation.
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