Tropical Journal of Pharmaceutical Research
Pharmacotherapy Group, Faculty of Pharmacy, University of Benin, Benin City, Nigeria
Vol. 15, No. 4, 2016, pp. 717-722
Bioline Code: pr16095
Full paper language: English
Document type: Research Article
Document available free of charge
Tropical Journal of Pharmaceutical Research, Vol. 15, No. 4, 2016, pp. 717-722
© Copyright 2016 - Tropical Journal of Pharmaceutical Research
Effect of β3-adrenoceptor on cardiac fibrosis in rat cardiac fibroblast cells and its potential mechanism|
Zhang, Yuan; Zhang, Hui; Ma, Yitong; Yang, Yining; Ma, Miaomiao; Zhu, Xiaoli & Wang, Li
To investigate the effect of β3-adrenoceptors (β3-AR) up-regulation on fibrosis in cardiac
fibroblast cells in rats and its potential mechanism.
Cardiac fibroblast cells (CFB) were isolated and identified from rats’ hearts. The β3-ARupregulated
cardiac fibroblast cells were constructed by lentiviral transfection technology. Thereafter, Ang
II was used to induce fibrosis in cardiac fibroblast cells, and subsequently, Western blot assay was
performed to investigate fibrosis related marker proteins (TGF-β, Smad-2, p-Smad-2, Col-I and Col-III)
in cardiac fibroblast cells.
β3-AR up-regulated cardiac fibroblast cells were successfully constructed. Furthermore, the
results show that up-regulation of β3-AR increased the expressions of TGF-β, p-Smad-2, Col-I and Col-
III proteins in Ang II treated cardiac fibroblast cells.
The results suggest that up-regulation of β3-AR aggravates fibrosis of cardiac fibroblast
cells. In other words, inhibition of β3-AR expressions in cardiac tissues would be beneficial for treating
cardiac fibrosis and its related cardiac diseases.
Cardiac fibrosis; TGF/Smads; Cardiac fibroblast cells; β3-AR; Col-I/III
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