[Protective effect of hydrogen sulfide on rats with myocardial ischemia/reperfusion injury and its mechanism].
OBJECTIVE
To explore the protective effect of hydrogen sulfide (H2S) on rats with myocardial ischemia/reperfusion injury (MIRI) and its related mechanism.


METHODS
Thirty male SD rats were randomly divided into 3 groups: control group, model group and H2S-treated group (n=10 in each). The MIRI model was established by ligating left anterior descending coronary artery for 40 minutes followed by reperfusion for 2 hours. Rats in H₂S-treated group were injected with 14 μmol/kg sodium hydrosulfide (NaHS) intraperitoneally before ischemia and reperfusion, respectively. After 24 hours of reperfusion, blood was collected from abdominal aorta and serum was separated. Then, the heart was removed. The myocardial histopathological changes were observed using HE staining. Serum levels of creatine kinase MB isozyme (CK-MB), lactate dehydrogenase (LDH) and cardiac troponin I (cTnI), as well as the activities of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione-peroxidase (GSH-Px) and catalase (CAT) in the homogenate of myocardium were examined using the kits. Myocardial interleukin (IL)-1β, IL-6, IL-18 and tumor necrosis factor-α (TNF-α) contents were detected by ELISA. The levels of intracytoplasm Keap 1 and intranuclear nuclear factor-erythroid 2-related factor 2 (Nrf2) and nuclear factor-κB (NF-κB) p65 in myocardium were measured using Western blotting.


RESULTS
H₂S administration markedly relieved the pathological injury of myocardium. In comparison with control group, serum CK-MB, LDH and cTnI levels, myocardial MDA activities, nuclear factor erythroid 2-related factor 2 (Nrf2) and NF-κB p65 levels in the nucleus, and myocardial contents of IL-1β, IL-6, IL-18 and TNF-α were significantly elevated, whereas myocardial SOD, GSH-Px and CAT activities as well as Keap 1 level in the cytoplasm were significantly reduced in model group. After H₂S treatment, serum CK-MB, LDH and cTnI levels, myocardial MDA activities, Keap 1 level in the cytoplasm, myocardial contents of IL-1β , IL-6, IL-18 and TNF-α, and NF-κB p65 levels in the nucleus decreased, but myocardial SOD, GSH-Px and CAT activities, and Keap 1 level in the cytoplasm increased as compared with model group.


CONCLUSIONS
Exogenous H₂S could confer protection against MIRI in mice. The mechanism might be related to the enhancement of antioxidative ability and the decrease of inflammatory factor release.
Department of Anesthesia, First Affiliated Hospital, University of South China, Hengyang 421001, China.
Yansheng
Y
Zhang
Department of Anesthesia, First Affiliated Hospital, University of South China, Hengyang 421001, China.
Liangyu
L
Peng
Department of Anesthesia, First Affiliated Hospital, University of South China, Hengyang 421001, China.
Xiaohua
X
Yu
D000818:Animals; D002374:Catalase / Q000235:genetics / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000235:genetics / Q000378:metabolism; D006801:Humans; D006862:Hydrogen Sulfide / Q000008:administration & dosage*; D020382:Interleukin-18 / Q000235:genetics / Q000378:metabolism; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism / Q000517:prevention & control; D020011:Protective Agents / Q000008:administration & dosage*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000235:genetics / Q000378:metabolism
D020382:Interleukin-18; D053583:Interleukin-1beta; D015850:Interleukin-6; D020011:Protective Agents; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D006862:Hydrogen Sulfide