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Objective To investigate the effects of emulsified isoflurane on myocardial apoptosis, and the expressions of Bcl-2 and Bax after hypoxia/reoxygenation in cultured myocardial cells of neonatal rats. Methods Myocardial hypoxia/reoxygenation model was established on cultured primary myocardial cells of neonatal rat. The myocardial cells were divided into four groups: the normal group, model group, fat milk group, and emulsified isoflurane group. The cellular morphologic changes and pulsatile frequency of each group were observed under inverted microscope and the ultrastructure of myocardial cells was observed under transmission electron microscope. The apoptotic rate of myocardial cells was determined by flow cytometry, the expression of bcl-2 mRNA and bax mRNA were detected by RT-PCR and the protein expressions of Bcl-2/Bax were observed by Western blot. Results The apoptotic rate were significantly decreased in both emulsified isoflurane and fat milk groups (P0.05). Conclusion Emulsified isoflurane and one of its components, fat milk,can inhibit myocardial apoptosis induced by hypoxia/reoxygenation in cultured myocardial cells. Emulsified isoflurane exerts its anti-apoptosis effect maybe through up-regulating Bcl-2 expressions and down-regulating Bax expressions.
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AIM: To observe the effects of interactions between captopril and aspirin on injured myocardial cells from neonate rats and its mechanism. METHODS: The injury model of cultured neonatal rat myocardial cells was developed. The activity of lactate dehydrogenase (LDH) and the level of nitric oxide (NO) were measured by LDH kits and Griess reagent respectively, the intracellular free calcium concentrations were measured with Fura-2/AM. RESULTS: Both captopril and aspirin could reduce obviously the activity of LDH and increase the level of NO in medium, but their combination produced significant antagonistic interactions. Captopril reduced obviously the intracellular free calcium concentrations in the injury model, but aspirin alone or in combination with captopril significantly increased it. CONCLUSION: Captopril and aspirin combination produced significant antagonistic interactions, the effects may be related to its actions of reducing the production of NO and increasing the intracellular free calcium concentrations.
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BACKGROUND: In order to elucidate toxic mechanism of the oxygen radicals on cultured rat myocardial cells, cytotoxic effect of oxygen radicals was evaluated by MTT assay. In addition protective effect of glutathione(GSH) on oxidant-induced cardiotoxicity was investigated on these cultures. METHODS: Myocardial cells derived from neonatal rats were cultured for 12 hours in the medium containing various concentrations of glucose oxidase(GO). Cell viability was measured by MTT assay and morphological changes of the myocardial cells were observed by light microscope. RESULTS: GO-mediated oxygen radicals remarkably decreased cell viability of cultured myocardial cells in a dose-and time-dependent manner. And also, GSH blicked GO-induced cardiotoxicity in these cultures. CONCLUSION: These results suggest that the oxygen radicals are tixic and the selective antioxidants such as GSH are effective in blocking against the oxidant-induced cardiotoxicity in cultures of the myocardial cells of neonatsl rats.
Subject(s)
Animals , Rats , Antioxidants , Cell Survival , Glucose , Glutathione , Reactive Oxygen SpeciesABSTRACT
BACKGROUND: It is known that methylmercury poisoning, Minamata disease is very toxic to human body. But, cardiotoxic mechanism of methylmercury is left unknown, Recent study has been reported that the cleavage of methylmercury produce oxygen radicals as well as methyl radicals, and also these radicals induce the release of excitotoxic amino acids(EAAs). So, oxygen radicals and EAA are regarded as a causative factors in the various diseases such as heart disease induced by toxicity of methylmercury. We studied to know the cardiotoxic effect of methylmercury on cultured myocardial cells derived from neonatal rat in order to evaluate the toxic mechanism of methylmercury. METHODS: Myocardial cells of neonatal rat were incubated with various concentrations of methylmercuric chloride for 1-96 hours. MTT90 and MTT50 values were measured and cell viability was determined by MTT assay. In addition, morphological study was performed by light microscope after cultured myocardial cells that were exposed to methymercuric chloride. RESULTS: MTT90 and MTT50 values were 1microM and 15microM of methylmercuric chloride in cultured myocardial cells of neonatal rat respectively. Exposure of cultured rat myocardial cells to methylmercuric chloride resulted in a significant cell death in a time-dependent manner. In the observation of morphological changes, cultured cells treated with methlymercuric chloride showed decrease of cell number and disconnection between cultured myocardial cells. CONCLUSION: These observation suggest that methylmercury has a severe myocardiotoxicity on cultured myocardial cells derived from neonatal rat by the decrease of cell viability and morphological changes.