Xie Ying-Hua, Zhang Nan, Li Lan-Fang, Zhang Qin-Zeng, Xie Li-Jun, Jiang Hong, Li Li-Ping, Hao Na, Zhang Jian-Xin
Department of Pharmacology, Hebei Medical University, Shijiazhuang, Hebei 050017, P.R. China.
Department of Pharmacology, Hebei Academy of Medical Sciences, Shijiazhuang, Hebei 050021, P.R. China.
Mol Med Rep. 2014 Oct;10(4):1907-14. doi: 10.3892/mmr.2014.2391. Epub 2014 Jul 17.
Hydrogen sulfide (H2S) is a signaling gasotransmitter, involved in various physiological and pathological processes. H2S-donating drugs have been tested to conjugate the beneficial effects of H2S with other pharmaceutical properties. It has been shown that the endogenous cystathionine-γ-lyase (CSE)/H2S pathway participates in myocardial ischemia injury in isolated hearts in rats. The present study aimed to investigate the cytoprotective action of H2S against acute myocardial ischemia injury in rats. Isolated rat hearts were perfused and subjected to ischemic conditions for 4 h. The hearts were assigned to five groups: Sham, model, infarct plus low-dose (5 µmol/l) NaHS, infarct plus middle-dose (10 µmol/l) NaHS and infarct plus high-dose (20 µmol/l) NaHS. The administration of NaHS enhanced the activity of CSE, increased the content of H2S and reduced infarct volumes following myocardial ischemia injury. Furthermore, the administration of NaHS attenuated the injury to organelles (including the mitochondria, nucleus and myofilaments) by reducing lactate dehydrogenase activity, decreasing the level of mitochondrial malondialdehyde and increasing the activities of superoxide dismutase and glutathione peroxidase in the ischemic myocardial mitochondria. These protective effects of H2S against myocardial ischemia injury appeared to be mediated by its antioxidant activities and the preservation of mitochondrial function.
硫化氢（H₂S）是一种信号气体递质，参与多种生理和病理过程。已对供H₂S药物进行测试，以将H₂S的有益作用与其他药物特性相结合。研究表明，内源性胱硫醚-γ-裂解酶（CSE）/H₂S途径参与大鼠离体心脏的心肌缺血损伤。本研究旨在探讨H₂S对大鼠急性心肌缺血损伤的细胞保护作用。对离体大鼠心脏进行灌注，并使其处于缺血状态4小时。将心脏分为五组：假手术组、模型组、梗死加低剂量（5 μmol/l）硫氢化钠（NaHS）组、梗死加中剂量（10 μmol/l）NaHS组和梗死加 高剂量（20 μmol/l）NaHS组。给予NaHS可增强CSE活性，增加H₂S含量，并减少心肌缺血损伤后的梗死体积。此外，给予NaHS可通过降低乳酸脱氢酶活性、降低线粒体丙二醛水平以及增加缺血心肌线粒体中超氧化物歧化酶和谷胱甘肽过氧化物酶的活性，减轻对细胞器（包括线粒体、细胞核和肌丝）的损伤。H₂S对心肌缺血损伤的这些保护作用似乎是由其抗氧化活性和线粒体功能的维持介导的。
