| Sphingosine-1-phosphate (S1P) is a immediated metobolites which produced from SM by sphingomyelinase. In addition, platelate is an important site where SIP synthesize and releases. S1P receptors is high homologous families of G protein coupling receptors. SIP1-SIP5 were subgrouped. S1P could show multiple bio-effects by introduction of specific receptors and coresponding signal transduction pathway. These bio-effects include inhibiton of cellular apoptosis, induction of growth and transmigration vascular endothelial cell, regulation of blood vessles development, regulation of immune response, promotion of skeletal system growth, and also concerns with growth and transmigration of tumor. It has been paid attention by people gradully for its involement of some physiolocal and pathologcal progress.Activation of phospholipase becomes more stronger at the time infarction. The amount of S1P becomes larger after degradation of membrane phopholipid. At the mean while, since the activation of agglutination platelet locally, the S1P would be realease more form platelet. It would lead to the concentration of SIP increasing at plasma and storing at myocardium locally. While S1P receptor distributed at the myocardium could bind with SIP tightly. Thus SIP is supposed to bind to it's own receptor then affect the process of infarction. However, less report about S1P function at the time of acute infarction has been published. Especially, the function and mechanism of S1P affect cardiocyte electriphysiologcial features during the period of acute infarction. Electriphysiological technique, surface electrocardiogram were applied. Parameters of cardiocyte action potential and membrane current of ion channels were determined as some indexes. The function and mechanism of S1P would be stuied on electriphysiological features of cardiocyte at the time of acute infarction. In order to reveal the effects of this substance on progress of myocardium infarction.Whole cell patch clamp technique was applied to study the L-type calcium current of ventricular myocyte in guinea pig. The holding potential was set at -50mV. From -50mV depolarizing to +60mV,10mV was stage jump and last 300ms appointed voltage. It has not been shown that the change of LCa has significant difference at the groups of the concentration of S1P (0.55μmol/L),S1P(1.1μmol/L )andS1P( 2.2μmol/L) compared to control group. LCa of S1P(1.1μmol/L)decreased from (0.513±0.067)nA to (0.509±0.055)nA. While LCa of S1P(2.2μmol/L)decreased from (0.522±0.041)nA to (0.516±0.069) nA. There is no significant difference compared to control group( P >0.05,n=6). The above results suggested that S1P show no effects on L-type calcium current of ventricular myocyte in guinea pigSingle-channel patch-clamp technique records the delayed rectifier K + currents of ventricular myocytes in guinea pig. The holding potential was set at -50mV. From -40mV depolarizing to +40mV, 20mV was stage jump and last 300ms appointed voltage. The results showed that S1P make the opening dwell time of delayed rectifier K+ currents of ventricular myocytes shorte to (2.7637±0.8595) s, extend the closing dwell time (7.3677±0.8733) s ,compared with the control group (5.3043±0.6473) s, (4.3633±0.2623) s, p <0.05. S1P make the open probability of the delayed rectifier K+ currents of ventricular myocytes t reduce (26.1897±8.1451)%, compared with the control group (50.2663±6.1339)%, p <0.05. Compared with the control group, there was no significant statistical difference (P> 0.05) in Suramin and S1P group. The above results suggested that S1P inhibit delayed rectifier potassium current of ventricular myocyte in guinea pig remarkably.It's mechanism may concern coupling of G-protein and S1P receptor.An experimental model of oxidative injury was established by using cultured neonatal rat cardiomyocytes.Cultured neonatal cardiomyocytes were divided into three groups randomly:①Normal group;②H2O2 group:in which cells were treated with H2O2 (0.3mmol/L) for 2h ;③S1P(0.55μmol/L )+ H2O2 group;④S1P(1.1μmol/L )+ H2O2 group;⑤S1P(2.2μmol/L )+ H2O2 group;An Olmpus inverted phase-contrast microscope was used to observe the growth condition , appearance and beating of cell. we observed cell of normol group grouth in good condition and beat regularly. After treatment with H2O2 , mostly cells were dead .we can see a great deal fragment of cell. The volum of the cell diminished and the beating became weak or even stopped compared with the control group. Cells of S1P+H2O2 group had a better groth condition and a highter survival rate compared with the H2O2 group.S1P can protect cardiomyocytes from H2O2 injury by improving cell antioxidant ability. |
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