摘要
目的：探讨N-乙酰基-丝氨酰-天门冬酰-赖氨酰-脯氨酸（AcSDKP）对大鼠矽肺纤维化模型肺组织中胶原含量、结缔组织生长因子（CTGF）和细胞外信号调节激酶1／2（ERK1／2）表达的影响。方法：选用非暴露式气管灌注法复制大鼠矽肺模型，并给予AcSDKP，采用羟脯氨酸测量法定量分析肺组织中总胶原蛋白的含量，免疫组织化学法、免疫印迹法检测肺组织内CTGF、phospho-ERK1／2及ERK1／2蛋白的表达。结果：AcSDKP治疗组胶原含量低于相对应的矽肺模型组。与相应的对照组相比，矽肺模型组大鼠肺组织内CTGF、phospho-ERK1／2蛋白表达均增加；与相应矽肺模型组相比，给予AcSDKP后，大鼠肺组织内CTGF、phospho-ERK1／2蛋白表达均明显降低。而各组间比较ERK1／2蛋白表达无明显改变。结论：AcSDKP可能通过阻断ERK1／2途径抑制了CTGF的表达，从而发挥抗矽肺纤维化的作用。
Objective： To investigate effect of N-acetyl-seryl-aspartyl-lysyl-proline （AcSDKP） on the collagen content and the expressions of connective tissue growth factor （CTGF） and ERK1/2 in the lungs of rats with silicosis. Methods： Rats were instilled with silica through trachea as silicotic models and administrated AcSDKP in the experiment. Collagen content was detected by hydroxyproline determination. The expression of CTGF, phospho-ERK1/2 and ERK1/2 was measured by immunohistochemistry and Western blot. Results： The content of collagen in the AcSDKP-treated group was less than that in the corresponding silicotic model group. Compared with the corresponding control group, the expressions of CTGF and phospho-ERK1/2 increased in the lung tissue of the silicotic model. Compared with the corresponding model group, the expressions of CTGF and phospho-ERK1/2 in the lung tissue reduced obviously after administration of AcSDKP. There was no significant expression of ERK1/2 in each group. Conclusion： AcSDKP possibly play an important role in anti-silicotic fibrosis by blocking the ERK1/2 signal transduction pathway to inhibit the expression of CTGF.
出处
《解剖学杂志》
CAS
CSCD
北大核心
2009年第4期432-436,共5页
Chinese Journal of Anatomy
基金
中华人民共和国人事部留学人员科技活动基金（国人厅发[2006]164号）
河北省自然科学基金（C2005000807）
唐山市新药基础研究重点实验室项目（04362001B-9）
