Tan Jian, Xia Ji-yi, He Hong-yan, Chen Feng, Fan Jun-ming, Ou San-tao, Liu Jian
Department of Urology, Affiliated Hospital, Luzhou Medical College, Luzhou, China.
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2012 Aug;28(8):808-10.
To explore the influence of angiotensin-(1-7) [Ang-(1-7)] on cell activation and extracellular matrix secretion in rat renal interstitial fibroblasts (NRK-49F) induced by aldosterone (ALD).
The NRK-49F cells were cultured in vitro, and then were divided into control group, ALD group, Ang-(1-7) group, and ALD+Ang-(1-7) group. When the cells were cultured for 48 h, the expression of α-smooth muscle actin (α-SMA) (a sign of cell activation) was detected by immunocytochemistry; the level of collagen type I (Col I ) in the cultured supernatant was measured by enzyme-linked immunosorbent assay (ELISA). When the cells were cultured for 30 min, the expressions of phosphorylated and total ERK1/2 (pERK1/2, tERK1/2) in the cell lysate were detected by Western blotting.
Compared with control group, the expressions of α-SMA, Col I and the Phos/Total ERK1/2 ratio in ALD group and ALD+Ang-(1-7) group increased significantly (P<0.05). Compared with ALD group, the expressions of α-SMA, Col I and the Phos/Total ERK1/2 ratio in ALD+Ang-(1-7) group decreased significantly (P<0.05).
Ang-(1-7) can inhibit ALD-induced cell activation and decrease the secretion of Col I in rat renal interstitial fibroblasts. Inhibition of ERK1/2 pathway may play an important role in this process.
探讨血管紧张素-（1-7）[Ang-（1-7）]对醛固酮（ALD）诱导的大鼠肾间质成纤维细胞（NRK-49F）细胞活化及细胞外基质分泌的影响。
体外培养NRK-49F细胞，然后分为对照组、ALD组、Ang-（1-7）组和ALD+Ang-（1-7）组。细胞培养48 h后，采用免疫细胞化学法检测α-平滑肌肌动蛋白（α-SMA，细胞活化标志）的表达；采用酶联免疫吸附测定（ELISA）法检测培养上清液中Ⅰ型胶原（Col Ⅰ）水平。细胞培养30 min后，采用蛋白质免疫印迹法检测细胞裂解液中磷酸化及总细胞外调节蛋白激酶1/2（pERK1/2、tERK1/2）的表达。
与对照组比较，ALD组和ALD+Ang-（1-7）组α-SMA、Col Ⅰ表达及Phos/Total ERK1/2比值明显升高（P<0.05）。与ALD组比较，ALD+Ang-（1-7）组α-SMA、Col Ⅰ表达及Phos/Total ERK1/2比值明显降低（P<0.05）。
Ang-（1-7）可抑制ALD诱导的大鼠肾间质成纤维细胞活化，并减少Col Ⅰ分泌。抑制ERK1/2通路可能在此过程中起重要作用。
