MAPK/ERK1与STAT3在脂多糖诱导的腺性膀胱炎动物模型中的表达

Expression of MAPK/ERK1 and STAT3 in a cystitis glandularis model of rats induced by exposure to lipopolysaccharide

目的研究丝裂原激活蛋白激酶(MAPK)成员之一ERK1与信号转导子与转录激活子3(STAT3)在内毒素脂多糖(LPS)诱导的大鼠腺性膀胱炎动物模型中的表达。方法成年雌性SD大鼠24只,建立腺性膀胱炎动物模型,免疫组织化学染色检测上皮组织中ERK1及STAT3的表达,用RT-PCR技术及Western blotting检测ERK1及STAT3基因及蛋白表达量的变化。结果 LPS可显著激活膀胱上皮细胞中ERK1及STAT3的表达,两种基因在转录水平上的相对表达量分别为1.99±0.12和1.71±0.08。结论 MAPK/ERK1及STAT3信号通路参与了LPS诱导的大鼠腺性膀胱炎的病理过程。

Objective To determine the expression of mitogen activated protein kinase /extracellular signal regulated kinase 1 （ MAPK/ERK1 ） and signal transducer and activator of transcription 3 （ STAT3 ） in cystitis glandularis （CG） models of rats induced by exposure to lipopolysaccharide （LPS）. Methods Twenty-four female Sprague-Dawley rats were used, 10 of which were catheterized and intravesically exposed to LPS for 8 weeks. Immunohistochemistry, RT- PCR and Western blotting methods were used to demonstrate the expression of ERK1 and STAT3 in sections of cystitis glandularis. Results Immunohistochemistry demonstrated that ERK1 and STAT3 were more intensive induced by LPS than those in the control. The relative expression of ERK1 and STAT3 of transcription were 1.99 ± 0. 12 and 1.71 ± 0.08, respectively. Conclusion The increased ERK1 and STAT3 suggest that MAPK/ERK1-STAT signaling pathway may participate the pathological process of CG induced by LPS in rats.