Subject(s)
Fatty Liver, Alcoholic/metabolism , NG-Nitroarginine Methyl Ester/pharmacology , Nitric Oxide Synthase/antagonists & inhibitors , Nitric Oxide/metabolism , Superoxide Dismutase/metabolism , Animals , Liver/metabolism , Male , Oxidation-Reduction , Random Allocation , Rats , Rats, Sprague-DawleyABSTRACT
OBJECTIVE: To examine whether urotensinII (UII) induces hypertrophy of neonatal rat cardiomyocytes cultured in vitro. METHODS: The primary cardiac myocytes cultured for 40 h followed by further culture in serum-free media for another 24 h were subjected to exposure to UII of varied concentrations for 24 h, after which the changes in the size of the cells were analyzed by flow cytometry with (3)H-leucine incorporation also measured. RESULTS: At the concentration of 1x10(-7) mol/L, UIIcould increase the size of the cultured cardiac myocardial cells (P=0.021) and 3H-Leucine incorporation (P=0.015). CONCLUSION: UII may induce hypertrophy of neonatal rat cardiac myocytes cultured in vitro.
Subject(s)
Cardiomegaly/chemically induced , Myocytes, Cardiac/drug effects , Urotensins/toxicity , Animals , Animals, Newborn , Cells, Cultured , Female , Immunohistochemistry , Male , Myocytes, Cardiac/pathology , Rats , Rats, Sprague-Dawley , Receptors, G-Protein-Coupled/analysisABSTRACT
OBJECTIVE: To observe the effect of urotensin II on cultured cardiac fibroblast collagen type I mRNA expression and proliferation, thereby to explore the role of urotensin II in myocardial remodeling in the event of cardiac failure. METHODS: Cardiac fibroblasts of neonatal Sprague-Dawley rats isolated by trypsin digestion method were stimulated by urotensin II at varied concentrations when the cells reached growth arrest. MTT assay was employed to measure the proliferation and determine the number of the cells, and reverse transcriptional (RT)-PCR used to detect the collagen mRNA expression. RESULTS: With the increase of urotensin II concentration, the optical density at 570 nm of the fibroblasts as shown by MTT assay first increased but then decreased, and remained at a significantly higher level in the cells treated with 1x10(-8) or 1x10(-9) mol/L urotensin II as compared with the control (P<0.05). The collagen type I mRNA levels of the cells treated with 1x10(-7), 1x10(-8) or 1x10(-9) mol/L urotensin II were significantly higher than that of the control cells (P<0.01). CONCLUSION: Urotensin II can directly induce cardiac fibroblast proliferation and significantly increase collagen type I mRNA expression, suggesting the crucial role of urotensin II in myocardial remodeling.
