title: Hydrogen sulfide reduces regional myocardial ischemia injury through protection of mitochondrial function.
abstract: 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.
authors.affiliation: Department of Pharmacology, Hebei Medical University, Shijiazhuang, Hebei 050017, P.R. China.
authors.forename: Ying-Hua
authors.initials: YH
authors.lastname: Xie
authors.affiliation: Department of Pharmacology, Hebei Medical University, Shijiazhuang, Hebei 050017, P.R. China.
authors.forename: Nan
authors.initials: N
authors.lastname: Zhang
authors.affiliation: Department of Pharmacology, Hebei Academy of Medical Sciences, Shijiazhuang, Hebei 050021, P.R. China.
authors.forename: Lan-Fang
authors.initials: LF
authors.lastname: Li
authors.affiliation: Department of Pharmacology, Hebei Academy of Medical Sciences, Shijiazhuang, Hebei 050021, P.R. China.
authors.forename: Qin-Zeng
authors.initials: QZ
authors.lastname: Zhang
authors.affiliation: Department of Pharmacology, Hebei Academy of Medical Sciences, Shijiazhuang, Hebei 050021, P.R. China.
authors.forename: Li-Jun
authors.initials: LJ
authors.lastname: Xie
authors.affiliation: Department of Pharmacology, Hebei Academy of Medical Sciences, Shijiazhuang, Hebei 050021, P.R. China.
authors.forename: Hong
authors.initials: H
authors.lastname: Jiang
authors.affiliation: Department of Pharmacology, Hebei Academy of Medical Sciences, Shijiazhuang, Hebei 050021, P.R. China.
authors.forename: Li-Ping
authors.initials: LP
authors.lastname: Li
authors.affiliation: Department of Pharmacology, Hebei Academy of Medical Sciences, Shijiazhuang, Hebei 050021, P.R. China.
authors.forename: Na
authors.initials: N
authors.lastname: Hao
authors.affiliation: Department of Pharmacology, Hebei Medical University, Shijiazhuang, Hebei 050017, P.R. China.
authors.forename: Jian-Xin
authors.initials: JX
authors.lastname: Zhang
mesh_terms: D000818:Animals; D005979:Glutathione Peroxidase / Q000378:metabolism; D006439:Hemodynamics; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D017202:Myocardial Ischemia / Q000378:metabolism / Q000473:pathology* / Q000517:prevention & control; D020011:Protective Agents / Q000494:pharmacology* / Q000627:therapeutic use; D051381:Rats; D017207:Rats, Sprague-Dawley; D013440:Sulfides / Q000494:pharmacology* / Q000627:therapeutic use; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D020011:Protective Agents; D013440:Sulfides; D008315:Malondialdehyde; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; C025451:sodium bisulfide