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作 者:蒋向荣[1] 陈治新[1] 张莉娟[1] 陈运新[1] 李丹[1] 陈丰霖[1] 黄月红[1] 王小众[1]
机构地区:[1]福建医科大学附属协和医院消化内科,福建福州350001
出 处:《中西医结合肝病杂志》2003年第3期154-157,共4页Chinese Journal of Integrated Traditional and Western Medicine on Liver Diseases
基 金:福建省教育厅资助课题(JA01070)
摘 要:目的:探讨胰岛素样生长因子-1(IGR-1)在实验性大鼠肝纤维化过程中的表达状况及白细胞介素-10(IL-10)对肝纤维化大鼠IGF-1表达的影响。方法:建立大鼠肝纤维化模型并行IL-10干预实验。分批从肝纤维化进程中不同阶段的对照组、CCl_4诱导肝纤维化模型组及IL-10干预肝纤维化组的大鼠中取肝脏组织,采用S-P免疫组织化学方法分别检测分析不同组及同组不同阶段大鼠肝组织中IGF-1的表达状况。结果:经CCl_4诱导成功建立大鼠肝纤维化模型。随着肝纤维化程度的进展,IGF-1在肝组织中阳性表达明显增强;经Ridit分析,对照组(38.1%)与肝硬化模型组(92.0%)组间比较IGF-1阳性表达均有显著性差异(P<0.01);IL-10干预肝纤维化组IGF-1阳性表达(71.4%)较肝纤维化模型组均明显减弱,经Ridit分析组间均有显著性差异(P<0.05),且随IL-10干预时间的延长,IGF-1在肝组织中阳性表达均逐渐减弱。结论:IGF-1随着肝纤维化程度的进展阳性表达增强,外源性IL-10可降低CCl_4诱导大鼠肝纤维化中IGF-1的表达。Objective: To study the expression of IGF-1 and its intervention by IL-10 in the course of experimental hepatic fibrosis. Methods: Experimental rat hepatic fibrosis model induced by CCl4 was established and the liver tissues were obtained from the control group, the model group and the IL-10 treated group in different period respectively. The expression of IGF-1 in different group and different phase in the development of hepatic fibrosis was measured by S-P immunohistochemistry. Results: The CCl4-induced experimental rat hepatic fibrosis model was established successfully. The positive expression of IGF-1 was increased obviously with the development of hepatic fibrosis, and the positive expression was mainly in the plasma and/or the membrane of hepatocytes. Ridit analysis indicated that there was significant difference between the positive expression of IGF-1 in control group (38.1%) and that in model group (92.0%, P<0.01), the positive expression in IL-10 treated group (71.4%) was decreased when compared with control group (P<0.05), and the positive expression decreasing gradually with the increasing IL-10 treatment time. Conclusion: The positive expression of IGF-1 in liver tissue was increased with the development of hepatic fibrosis, and ectogenic IL-10 restrained the expression of IGF-1 in liver fibrosis induced by CCl4.
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