摘要
目的:观察肺肠微生态及TGF-β1/Smads/ERK信号蛋白在溃疡性结肠炎大鼠肺损伤过程中的变化,探讨溃疡性结肠炎大鼠肺损伤的机制。方法:以三硝基苯磺酸(TNBS)构建溃疡性结肠炎动物模型,首次造模后第8、29、50天行肺部和肠道菌群的菌落鉴定及计数,用HE染色观察肺肠组织病理变化并评分,电镜观察组织超微结构,免疫组化法检测肺、结肠组织TGF-β1/Smads蛋白表达,Western Blot法检测ERK1/2、p-ERK1/2信号蛋白表达。结果:与正常组比较,模型组大鼠肺肠组织均出现病变,肺肠组织病理评分逐渐升高,肺肠部分菌群呈现同步规律性变化,肺肠组织TGF-β1、Smads、ERK1/2、p-ERK1/2蛋白表达增加。结论:溃疡性结肠炎大鼠可出现肺损伤,其机制可能与肺肠微生态改变及TGF-β1/Smads/ERK信号通路激活有关。
Objective： By observation of the changes of lung-intestines microecology and TGF- β1/Smads/ERK signaling pathway in process of lung injury of rats with ulcerative colitis, to explore the mechanism of lung injury of rats with ulcerative colitis. Methods： The ulcerative colitis （UC） rat model was replicated by trinitrobenzene sulfonic acid （TNBS）. The identification and count of bacterial colony in lung and intestines were conducted at 8, 29 and 50 days after establishing the model. H＆E staining was used to observe the pathological changes of lung and intestines tissues. The electron microscopy was used to observe the ultrastructure of lung and intestines tissues. The immunohistochemistry was used to detect the expression of TGF- β1/ Smads protein. Western blot method was used to detect the protein expressions of ERK1/2, p-ERKI/2. Results： The pathological changes of the lung and intestines tissues in model group were obvious observed, compared with those in the normal group. The pathological scores in model group were higher than that in the normal group. A part of microflora in lung tissues presented the synchronization with that in intestines tissue. The protein expressions of TGF- β1, Smads, ERKI/2, and p-ERKI/2 in model group were higher than those in the normal group. Conclusions： The mechanism of lung injury of rats with ulcerative colitis may be related to the changes of lung-intestines microecology and activate the TGF- β1/Smads/ERK signaling pathway.
出处
《中华中医药杂志》
CAS
CSCD
北大核心
2014年第11期3555-3559,共5页
China Journal of Traditional Chinese Medicine and Pharmacy
基金
国家重点基础研究发展计划(973计划)(No.2009CB522706)~~
