黄芩黄素减轻脱氧胆酸对食管上皮细胞损伤机制的探讨  

Baicalein attenuates deoxycholate-induced injury in human esophageal epithelial cells

作　　者：柳刚[1] 张玲[1] 郭晓军[2] 李桂香[1] 邹多武[1] 

机构地区：[1]第二军医大学附属长海医院消化内科,上海200433 [2]济南军区青岛第二疗养院干部二科,山东青岛266071

出　　处：《东南国防医药》2015年第2期113-115,145,共4页Military Medical Journal of Southeast China

基　　金：国家自然基金青年科学基金(81200273)

摘　　要：目的考察黄芩黄素(Baicalein)对脱氧胆酸诱导的人食管黏膜上皮细胞损伤的治疗作用。方法原代培养人食管黏膜上皮细胞,使用脱氧胆酸(deoxycholate,500μmol/L)进行刺激,同时给以不同浓度的黄芩黄素(1μmol/L,10μmol/L)进行干预治疗。12 h后,采用Western blotting和ELISA等方法观察细胞凋亡及炎症相关指标的变化。结果黄芩黄素治疗抑制脱氧胆酸诱导的细胞凋亡,剂量依赖地降低了caspase-3剪切体的生成和Bax蛋白的表达,同时增加Bcl-2蛋白的表达;黄芩黄素亦治疗剂量依赖地抑制了脱氧胆酸诱导的炎症因子白介素8(IL-8)和巨噬细胞趋化性和激活性因子(macrophage chemoattractant protein 1,MCP-1)的生成,抑制了脱氧胆酸诱导的食管上皮细胞中诱导型一氧化氮合酶(inducible nitric oxide synthase,i NOS)的蛋白表达和细胞中的一氧化氮(nitric oxide,NO)的生成。结论黄芩黄素通过抑制炎症,抑制i NOS/NO通路,减少凋亡,从而减轻了脱氧胆酸诱导的人食管黏膜上皮细胞的损伤。Objective The present study was designed to investigate whether Baicalein protected against deoxycholate-induced injury in human esophageal epithelial cells.Methods Primary cultured human esophageal epithelial cells were stimulated with deoxycholate（500 μmol / L）,and treated with Baicalein（1 μmol / L,10 μmol / L） simultaneously.12 hours later,the cells were collected for analysis of inflammation and apoptosis by Western blotting and ELISA.Results Baicalein treatment reduced formation of cleaved caspase-3 and protein expression of Bax and enhanced protein expression of Bcl-2,dose-dependently,indicating that Baicalein suppressed apoptosis induced by deoxycholate.Baicalein treatment suppressed deoxycholate-induced formation of pro-inflammatory cytokines including IL-8 and macrophage chemoattractant protein 1（MCP-1）.Baicalein treatment suppressed deoxycholate-induced upregulation of protein expression of inducible nitric oxide synthase（i NOS） and reduced intracellular nitric oxide（NO） levels.Conclusion Baicalein attenuated deoxycholate-induced injury in human esophageal epithelial cells,via suppressing apoptosis,inflammation,and i NOS / NO.

关 键 词：黄芩黄素 脱氧胆酸 食管黏膜上皮细胞 凋亡 炎症 诱导性一氧化氮合酶 

分 类 号：R571[医药卫生—消化系统] R932[医药卫生—内科学]