Hydrogen sulfide reduces regional myocardial ischemia injury through protection of mitochondrial function
Autor: | Qin‑Zeng Zhang, Hong Jiang, Ying‑Hua Xie, Nan Zhang, Na Hao, Jianxin Zhang, Lan‑Fang Li, Li‑Ping Li, Li‑Jun Xie |
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Rok vydání: | 2013 |
Předmět: |
Male
Cancer Research Pathology medicine.medical_specialty Antioxidant medicine.medical_treatment Myocardial Ischemia Endogeny Mitochondrion Pharmacology Sulfides Protective Agents Biochemistry Superoxide dismutase Rats Sprague-Dawley chemistry.chemical_compound Lactate dehydrogenase Malondialdehyde Genetics medicine Animals Molecular Biology chemistry.chemical_classification Glutathione Peroxidase biology business.industry Superoxide Dismutase Glutathione peroxidase Hemodynamics equipment and supplies Mitochondria Rats Oncology chemistry Apoptosis biology.protein Molecular Medicine business |
Zdroj: | Molecular medicine reports. 10(4) |
ISSN: | 1791-3004 |
Popis: | 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. |
Databáze: | OpenAIRE |
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