Objective      To investigate the effects of angiotensin1-7 (Ang1-7) on rat ventricular fibroblasts induced by angiotensinⅡ (AngⅡ).       Methods      The ventricles from 1~3-day-old Sprague-Dawley rats were digested with trypsin and collagenase type 2. The isolated ventricular fibroblasts were randomly divided into 4 groups: contro

l group

AngⅡ group

Ang1-7 group

and AngⅡ+Ang1-7 group. The control group

AngⅡ group and Ang1-7 group were treated with serum free DMEN

AngⅡ and Ang1-7

respectively. The AngⅡ+Ang1-7 group was pre-incubated with Ang1-7 for 30 min and then treated with AngⅡ. Fibroblasts were identified by immunofluorescence assay. CCK-8 assay was used to measure the proliferation of fibroblasts. Western blot assay was used to detect the expression of Rac1

Rad

gp91

phox

(Nox2)

P65 and connective tissue growth factor (CTGF). Real-time PCR was performed to quantify the mRNA expression of collagenⅠ (ColⅠ)

collagen Ⅲ (Col Ⅲ) and fibronectin.       Results      AngⅡcould promote proliferation of fibroblasts which could be inhibited by Ang1-7 (P0.05). Compared with the control group

the expression levels of Rac1

Nox2

P65 and CTGF were increased and that of Rad was decreased in the AngⅡgroup (P0.05)

while the mRNA levels of ColⅠ

Col Ⅲ and fibronectin were increased in the AngⅡ group (P0.05). Compared with the AngⅡgroup

the expression levels of Rac1

Nox2

P65 and CTGF were decreased and that of Rad was increased in the AngⅡ+Ang1-7 group (P0.05)

while the mRNA levels of ColⅠ

Col Ⅲ and fibronectin were decreased in the AngⅡ+Ang1-7 group (P0.05).       Conclusion      With the existance of AngⅡ

Ang1-7 plays a protective role in the ventricular fibroblasts. It inhibits the production of extracellular matrix through regulating Racl

Rad and downstream proteins.