RESUMO
AIM Taurine was reported neuroprotective under several ischemic models in vivo. In this study, the direct effect of taurine against oxygen-glucose deprivation (OGD) inducing acute neuronal injury and the underlying mechanisms in vitro were investigated. METHODSFour hours OGD was used to induce in vitro ischemic injury in rat cortical neurons. Taurine 5, 10 and 20 mmol·L-1 was added 20 h before and during 4 h OGD period respectively. Mortality rate of neuron was assayed by MTT and flow cytometry methods. Level of neuronal [Ca2+]i was detected by Fura 2/AM loading. Amino acid concentrations in culture media were measured by high performance liquid chromatography. RESULTS Under OGD conditions, neuronal death was markedly increased, and the levels of neuronal [Ca2+]i and extracellular glutamate level were enhanced obviously. Taurine pretreatment obviously decreased the percentage of neuronal death induced by OGD. In addition, abnormal elevation of neuronal [Ca2+]i and extracellular glutamate level induced by OGD both were markedly repressed by taurine. CONCLUSION Taurine can alleviate rat cortical neuron injury induced by OGD, the mechanisms were likely due to repressing calcium overload and inhibiting excessive release or leakage of glutamate under such conditions.
RESUMO
AIM To investigate whether dipfluzine (Dip) possesses antiarrhythmic effect on experimental arrhythmias and effect on cytosolic calcium in ventricular myocytes of guinea-pig. METHODS Experimental arrhythmias were induced by strophanthin G infusion through jugular vein in guinea-pigs and by myocardial ischemia-reperfusion (I-R) in rats respectively. Cytosolic calcium concentration ([Ca2+]i) of isolated guinea-pig ventricular myocytes was examined with laser confocal scanning microscope. RESULTSIn guinea-pigs pretreatment with Dip 20 mg·kg-1 increased the dosages of strophanthin G required to induce ventricular premature contraction (VP), ventricular tachycardia (VT), ventricular fibrillation (VF) and cardiac arrest (CA), pretreatment with Dip 10 mg·kg-1 increased the dosages of strophanthin G required to induce VP. In the I-R-induced arrhythmic model of rats, Dip 20 mg·kg-1 decreased the number of rats exhibiting VT, VF and CA, and the number of rats exhibiting VF and CA was decreased by Dip 10 mg·kg-1. Both Dip and verapamil (Ver) decreased [Ca2+]i of the ventricular myocytes in normal Tyrode′s solution. The Ca2+ overload evoked by high extracellular Ca2+ levels was inhibited by Dip and Ver, and the prophylactic effect of Dip was less than that of Ver, while the curative effect of Dip was more obvious than that of Ver. CONCLUSION Dip has antiarrhythmic effect, which is likely related to the modulation on the intracellular calcium homeostasis.