Effects of taurine on proliferation of rat cardiac fibroblast.
- Author:
Kuang REN
1
;
Yan-Chun WANG
;
Shi-Jie YANG
Author Information
1. School of Basic Medicine, Jilin Medical College, Jilin 132013, China.
- Publication Type:Journal Article
- MeSH:
Angiotensin II;
pharmacology;
Animals;
Animals, Newborn;
Cell Cycle;
drug effects;
Cell Proliferation;
drug effects;
Cells, Cultured;
Collagen Type I;
metabolism;
Collagen Type III;
metabolism;
Fibroblasts;
cytology;
metabolism;
Myocytes, Cardiac;
cytology;
metabolism;
Nitric Oxide;
metabolism;
Protein Kinase C-alpha;
metabolism;
Rats;
Rats, Wistar;
Signal Transduction;
drug effects;
Taurine;
pharmacology
- From:
Acta Pharmaceutica Sinica
2008;43(6):591-595
- CountryChina
- Language:Chinese
-
Abstract:
This project aimed to investigate the effect of taurine on nitric oxide (NO) and protein kinase C alpha (p-PKCalpha) in the proliferation of cultured neonatal rat cardiac fibroblast (CFb) induced by angiotensin II (Ang II), and to explore the effect of taurine on the signal transduction pathway in CFb proliferation. The cultured neonatal rats CFb were isolated by trypsin digestion method. The proliferation of CFb was induced by Ang II and detected by thiazole blue (MTT) colorimetric assay. The levels of collagen I and collagen III were measured by the ELISA. Cell cycle was analyzed by flow cytometry. The change of NO content was measured by nitric acid reductase method and the protein express of p-PKCalpha in cells was determined by Western blotting technology. Among the concentration of 40 - 160 mmol x L(-1), taurine could not only prevent the synthesis of collagen and the proliferation of CFb stimulated by angiotensin II, but also block CFb in the G0/G1 phase from entering the S phase, resulting in more cells in the G0/G1 phase and fewer in the S phase (P < 0.05, P < 0.01). Taurine significantly increased NO level and inhibited p-PKCalpha expression in CFb (P < 0.05, P < 0.01). The inhibitory effects of taurine on CFb proliferation and collagen synthesis might be due to inhibition of p-PKCalpha expression and NO content increase.
