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作 者:任婷婷[1] 贺红焰[2] 喻小兰 樊均明[1] 谭剑[1] 刘建[1]
机构地区:[1]泸州医学院附属医院肾内科,四川泸州646000 [2]泸州医学院附属医院病理科,四川泸州646000 [3]泸州医学院附属医院 [4]泸州市龙马潭妇幼保健院,四川泸州646000
出 处:《细胞与分子免疫学杂志》2013年第6期593-596,共4页Chinese Journal of Cellular and Molecular Immunology
基 金:国家自然科学基金(30771008)
摘 要:目的观察血管紧张素-(1-7)[Ang(1-7)]对氯化钴(Co)诱导的低氧状态下正常大鼠近端肾小管上皮细胞(NRK52E)间质转分化的影响并探讨其可能机制。方法体外培养NRK52E细胞,分为对照组、Co组、Ang-(1-7)组、Co+Ang-(1-7)组,培养6 d。免疫细胞化学染色法检测NRK52E细胞低氧诱导因子-lα(HIF-lα)和α-平滑肌肌动蛋白(α-SMA)的表达情况;Western blot法、细胞免疫化学染色法检测p-ERK1/2蛋白表达水平;酶联免疫吸附法检测细胞上清液Ⅰ型胶原蛋白(Col-Ⅰ)的含量。结果 6 d后,与对照组比较,Co组与Co+Ang-(1-7)组细胞HIF-1α、α-SMA、ColⅠ及p-ERK1/2表达量显著增加(P<0.05);与Co组比较,Co+Ang-(1-7)组细胞HIF-1α、α-SMA、ColⅠ及p-ERK1/2表达量明显减少(P<0.05)。结论 Ang-(1-7)可抑制Co诱导的低氧状态下肾小管上皮细胞间质转分化,减少细胞外基质的生成,可能是通过p-ERK1/2信号通路实现的。Objective To investigate the effect of angiotensin-(1-7) [ Ang(1-7) ] on the transdifferentiation of normal rat kidney proximal tubulαr epithelia cells (NRK52E) under hypoxic condition induced by cobaltous chloride (Co) and the under- lying mechanism. Methods NRK52E cells were divided into control group, Co group, Co +Ang-(1-7) group and Ang-(1-7) group and cultured for 6 d. Expression levels of hypoxiα-inducible factor-lα (HIF-lα) and α-smooth muscle actin (α-SMA) were detected by immunocytochemistry. Immunohistochemistry and Western blotting were used to determine the expression of p-ERK1/2 and ELISA to measure the content of collαgen type 1 (Col I ) in the culture supernatant. Results Compared with the control group, the expressions of HIF-lα, α-SMA, Col I and p-ERK1/2 in the Co group and the Co + Ang-(1-7) group increased significantly (P 〈0.05) 6 d lαter. Compared with the Co group, the expressions of HIF-lα, α-SMA, Col l and p-ERKI/2 in the Co + Ang-(1-7) group decreased significantly ( P 〈 0. 05). Conclusion Ang-(1-7) can inhibit Co-in- duced rats' tubulαr epithelial-to-mesenchymal transition and reduce the production of extracellulαr matrix. Inhibition of ERK1/ 2 pathway may plαy an important role in this process.
关 键 词:上皮间质转分化 低氧诱导因子-lα 低氧 血管紧张素-(1-7)
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