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Effects of Scutellarin on the Proliferation of Cardiac Fibroblasts in Neonate Rats Induced by Angiotensin Ⅱ and Signal Pathway of ERK1/2 and p38 MAPK / 中国药房
China Pharmacy ; (12): 629-633, 2018.
Article in Chinese | WPRIM | ID: wpr-704642
ABSTRACT

OBJECTIVE:

To study the effects of scutellarin on the proliferation of cardiac fibroblasts (CFs) in neonate rats induced by angiotensin Ⅱ (ANG Ⅱ) and signal pathway of extracellular regulated protein kinase (ERK1/2) and p38 mitogen activated protein kinase (p38 MAPK).

METHODS:

CFs of neonatal rat were isolated and cultured in vitro, and then divided into blank group (blank culture medium), Ang Ⅱ group (10-7 μmol/L), 50 μmol/L scutellarin group and Ang Ⅱ (10-7 μmol/L)+5, 10, 20, 50 μmol/L scutellarin groups. After cultured for 48 h, CCK-8 assay was used to detect the proliferation ability of cells. Other cells were selected and divided into blank group (blank culture medium), Ang Ⅱ group (10-7 μmol/L) and Ang Ⅱ +5, 10, 20, 50 μmol/L scutellarin groups. After cultured for 48 h, mRNA expression of Col I, Col Ⅲ and α-SMA in cells and hydroxyproline (HYP) content in cell culture fluid were detected; phosphorylation levels of ERK1/2 and p38 MAPK in cells were also detected.

RESULTS:

5, 10, 20, 50 μmol/L scutellarin could significantly inhibit the proliferation of CFs induced by Ang Ⅱ (P<0. 05), and decreased mRNA expression of Col I, Col Ⅲ and α-SMA in CFs induced Ang Ⅱ (P<0. 05). 5, 10, 20, 50 μmol/L scutellarin could significantly inhibit the increase of HYP content and the phosphorylation of ERK1/2 and p38 MAPK after induced by Ang Ⅱ (P<0. 05), in dose-dependent manner.

CONCLUSIONS:

Scutellarin inhibits the proliferation of CFs induced by Ang Ⅱ, the mechanism of which may be associated with reduction of ERK1/2 and p38 MAPK phosphorylation.

Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: China Pharmacy Year: 2018 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: China Pharmacy Year: 2018 Type: Article