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作 者:姜琳[1] 孙灿林[1] 肖蔚[2] 蒋小芹[2] 李慧[3] 于鸿[2]
机构地区:[1]泰州市人民医院麻醉科,江苏泰州225300 [2]泰州市人民医院病理科,江苏泰州225300 [3]复旦大学上海医学院病理系,上海200032
出 处:《江苏大学学报(医学版)》2011年第2期143-146,F0003,共5页Journal of Jiangsu University:Medicine Edition
基 金:上海市科委发展基金重点资助项目(01JC14018);泰州市311工程人才基金资助项目(201036)
摘 要:目的:研究IFN-γ对Thy1肾炎模型大鼠肾组织Sm ad7及Ⅳ型胶原表达的影响,从而为阐明IFN-γ抗肾纤维化机制及治疗肾纤维化提供理论和实验依据。方法:制备大鼠抗胸腺细胞血清(antithymocyte serum,ATS)肾炎模型,经尾静脉一次注射IFN-γ15万IU/kg,采用Northern b lot及免疫组化检测病变肾组织Sm ad7、Ⅳ型胶原的表达水平。结果:注射IFN-γ的ATS肾炎模型大鼠肾组织内Sm ad7的表达增加,Ⅳ型胶原mRNA的表达明显减少。结论:IFN-γ可能是通过上调Sm ad7表达而抑制肾组织Ⅳ型胶原表达的机制,对肾小球纤维化起抑制作用。Objective: To investigate the mechanism of IFN-γ antifibrosis and provide value clues for searching and developing new approaches to the prevention and treatment of organfibrosis,the expression of Smad7 and type Ⅳ collagen was detected in renal tissue of rat ATS glomerulonephritis.Methods: Rat antithymocyte serum glomerulonephritis model was built successfully adopting injection of IFN-γ 15×104 IU/kg vie tail vein once time.Northern blot and immunohistochemistry were employed to identify protein and mRNA expression of Smad7 and type Ⅳ collagen(Col Ⅳ) in renal tissue of rat ATS glomerulonephritis,respectively.Results: IFN-γ could increase the expression of Smad7 and decrease the expression of Col Ⅳ in renal tissue of rat ATS glomerulonephritis.Conclusion: It is possible that IFN-γ can alleviate the development of glomeruli fibrosis by the mechanism of upregulating the expression of Smad7,then downregulating the expression of Col Ⅳ.
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