Inhibitory effect of hydrogen sulfide on cardiac fibroblast proliferation.
- Author:
Jun LIU
1
;
Dan-Dan HAO
;
Yi-Chun ZHU
Author Information
1. Department of Physiology and Pathophysiology, Shanghai Medical College, Fudan University, Shanghai 200032, China.
- Publication Type:Journal Article
- MeSH:
Angiotensin II;
pharmacology;
Animals;
Animals, Newborn;
Cell Proliferation;
drug effects;
Cells, Cultured;
Depression, Chemical;
Fibroblasts;
cytology;
Hydrogen Sulfide;
pharmacology;
Male;
Myocardium;
cytology;
Rats;
Rats, Sprague-Dawley;
Reactive Oxygen Species;
metabolism
- From:
Acta Physiologica Sinica
2011;63(4):353-358
- CountryChina
- Language:Chinese
-
Abstract:
The aim of the present study was to investigate the role of hydrogen sulfide (H(2)S) in the proliferation of neonatal rat cardiac fibroblasts (NRCFs). Proliferation of NRCFs was induced by the presence of fetal bovine serum (FBS) or angiotensin II (Ang II) at various concentrations. The concentration-dependent effect of NaHS (donor of H(2)S) on NRCFs proliferation was examined. NRCFs proliferation was assessed by 5'-bromo-2'-deoxyuridine (BrdU) incorporation method. Reactive oxygen species (ROS) level was measured using the dye probe, 2', 7'-dichlorofluorescein diacetate (DCFH-DA). The results showed that FBS- or Ang II-induced NRCFs proliferations were inhibited with the treatment of relatively high concentrations of NaHS (5 × 10(-5) mol/L, 1 × 10(-4) mol/L), but FBS-induced proliferation was increased by low concentration of NaHS (1 × 10(-5) mol/L). Two or 6 h of Ang II (1 × 10(-7) mol/L) treatment caused an increase of ROS level in NRCFs, while this increase was inhibited with NaHS (1 × 10(-4) mol/L) treatment. These results suggest that H(2)S is an inhibitor of cardiac fibroblast at a certain concentration range. This inhibitory effect may be mediated by a reduction in intracellular ROS production.
