The study on protective effect of sphingosine-1-phosphate in cardiomyocytes.
- Author:
Lei YUAN
1
;
Wen-jie ZHANG
;
Duo-duo ZHANG
;
Chun-yan ZHAO
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Animals, Newborn; Apoptosis; drug effects; Cell Hypoxia; Cells, Cultured; Female; Lysophospholipids; pharmacology; Male; Membrane Potential, Mitochondrial; drug effects; Myocardial Reperfusion Injury; prevention & control; Myocytes, Cardiac; cytology; Oncogene Protein v-akt; metabolism; Phosphatidylinositol 3-Kinases; metabolism; Primary Cell Culture; Protective Agents; pharmacology; Rats; Signal Transduction; Sphingosine; analogs & derivatives; pharmacology
- From: Chinese Journal of Applied Physiology 2011;27(3):320-323
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the mechanism of protective effect of Sphingosine-1-phosphate(S1P) in cultured neonatal rat cardiomyocytes dining simulated hypoxia/reoxygenation.
METHODSOn the basis of culturing neonatal rat cardiomyocytes, the model of hypoxia-reoxygennation was built by using method of Liquid Paraffin covering, the impact of S1P on apoptosis and p-Akt and mitochondrial membrane potential were studied by using method of Propidine Iodide staining and Western blot and Bhodanmine123 staining.
RESULTSSiP could reduce apoptosis rate (P < 0.01) and stabilize the mitochondrial membrane potential (P < 0.05) and improved the level of p-Akt1 (P < 0.01) in hypoxia/reoxygenation cardiomyocytes significantly. But wonnannin could block these effects of S1P partially.
CONCLUSIONSiP can obviously restrain apoptosis in curtured rat neonatal cardiomyocytes during simulated hypoxia/reoxygenation. Stabilization of mitochondrial membrane potential by P13K-AM signaling pathway is likely to play a role in protective action of S1P.