【摘要】 目的探讨硫化氢(H2S)对体外培养乳鼠心肌细胞氧化损伤的保护作用及其机制。方法用低浓度过氧化氢诱导原代培养乳鼠心肌细胞氧化损伤模型,观察细胞形态结构,测定培养介质中乳酸脱氢酶(LDH)活力、细胞内丙二醛(MDA)含量、谷胱甘肽(GSH)和γ-谷氨酰半胱氨酸合成酶(-γGCS)活力。结果过氧化氢对心肌细胞有明显的损伤作用,H2S可使培养介质中的LDH活力和MDA水平显著下降,能通过加强-γGCS活力显著增加细胞内GSH水平。结论H2S对过氧化氢致心肌细胞损伤有保护作用,其机制之一可能是通过增加抗氧化剂GSH的生成。更多还原

【Abstract】 Objective To determine whether the administration of H2S is able to protect cardiomyocytes against oxidative stress.Methods An experimental model of oxidative injury was established by using cultured neonatal rat cardiomyocytes.Myocyte damages were estimated by lactate dehydrogenase(LDH) release and ultrastructural morphological alteration.Malondialdehyde(MDA) content was measured as an index of lipid peroxidation.Results H2S treatment significantly decreased LDH leakage and MDA production,and could increase the glutathione levels,which normally decreased during the cell death cascade by enhancing the activity of γ-glutamyl cysteine synthetase.These observations suggested that protection of cardiomyocytes by H2S required the increase in glutathione levels.Conclusions Pretreatment with H2S could protect cardiomyocytes from induced injury and the beneficial effect may be related to its increasing production of the antioxidant glutathione.更多还原