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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。
Objective To investigate the protective effect of hydrogen sulfide (H2S) on oxidative damage of cultured neonatal rat cardiomyocytes and its mechanism. Methods Primary cultured neonatal rat cardiomyocytes were induced to oxidative damage by low concentration of hydrogen peroxide. Morphology and structure were observed. The activities of lactate dehydrogenase (LDH), malondialdehyde (MDA), glutathione Peptide (GSH) and γ-glutamylcysteine synthetase (-γGCS) activity. Results Hydrogen peroxide had a significant damage on cardiomyocytes. H2S could significantly decrease the activity of LDH and MDA in culture medium and increase the intracellular GSH level by enhancing the activity of -GCS. Conclusions H2S may have a protective effect on the injury of cardiomyocytes induced by hydrogen peroxide. One of the mechanisms may be through increasing the production of GSH.