title: [Protective effect of hydrogen sulfide on mice with experimental viral myocarditis and its mechanism].
abstract: OBJECTIVE
  To explore the protective effect of hydrogen sulfide (H2S) on viral myocarditis (VMC) mice and its mechanism.
  
  
  METHODS
  Seventy BALB/c mice were randomly divided into 4 groups: normal control group (n=10), myocarditis group (n=20), DL-propargylglycine (PAG) group (n=20) and sodium hydrosulfide (NaHS) group (n=20). Mice in the latter three groups were inoculated with 0.1 mL Eagle's solution containing Coxsackievirus B3 (CVB3) intraperitoneally; whereas those in normal control group were treated with 0.1 mL Eagle's solution. On the day of inoculation, mice in PAG and NaHS groups received intraperitoneal administration with 40 mg/kg PAG and 50 μmol/kg NaHS, respectively; however, those in the other two groups were treated with PBS instead. PAG, NaHS or PBS were given one time for one day and persisted for 14 days. On day 15, all mice were killed after weighing body mass (BM). The mortality was compared among groups. Serum was separated and serum cardiac troponin I (cTnI) levels were detected using ELISA. The heart was removed and weighed to calculate heart mass (HM). Histological cross sections of heart were stained with hematoxylin-eosin, and myocardial histopathologic scores were counted under optical microscope. The activities of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione-peroxidase (GSH-Px) and catalase (CAT) in the homogenate of myocardium were examined. Myocardial interleukin (IL)-1β, IL-6 and tumor necrosis factor-α (TNF-α) contents were detected by ELISA. The expression level of myocardial nuclear factor-κB (NF-κB) p65 in the nucleus was examined using Western blotting.
  
  
  RESULTS
  Compared with normal control group, the HM/BM, serum cTnI levels, myocardial MDA activity, NF-κB p65 expression level in the nucleus and myocardial contents of IL-1β, IL-6 and TNF-α were elevated, but myocardial SOD, GSH-Px and CAT activities were reduced in myocarditis group (P<0.05 or P<0.01). In comparison with myocarditis group, HM/BM, serum cTnI levels, myocardial histopathologic scores, myocardial MDA activity, NF-κB p65 expression level in the nucleus and myocardial contents of IL-1β, IL-6 and TNF-α significantly increased while myocardial SOD, GSH-Px and CAT activities significantly decreased in PAG groups (P<0.05). There was no significant difference in the mortality between PAG group and myocarditis group (P>0.05). The mortality, HM/BM, serum cTnI levels, myocardial histopathologic scores, myocardial MDA activity, NF-κB p65 expression level in the nucleus and myocardial contents of IL-1β, IL-6 and TNF-α were lower, while myocardial SOD, GSH-Px and CAT activities were higher in NaHS group than in myocarditis group (P<0.05).
  
  
  CONCLUSIONS
  H2S can produce effective protection against VMC in mice. The mechanism may be associated with enhancing antioxidative ability and inhibiting inflammatory response.
authors.affiliation: Department of Clinical Medicine, Huaihua Medical College, Huaihua 418000, China.
authors.forename: Hong
authors.initials: H
authors.lastname: Qian
authors.affiliation: Department of Clinical Medicine, Huaihua Medical College, Huaihua 418000, China.
authors.forename: Lijing
authors.initials: L
authors.lastname: Liu
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002374:Catalase / Q000378:metabolism; D003384:Coxsackievirus Infections / Q000378:metabolism / Q000517:prevention & control* / Q000821:virology; D004770:Enterovirus / Q000502:physiology; D004797:Enzyme-Linked Immunosorbent Assay; D005979:Glutathione Peroxidase / Q000378:metabolism; D006367:HeLa Cells; D054884:Host-Pathogen Interactions / Q000187:drug effects; D006801:Humans; D006862:Hydrogen Sulfide / Q000494:pharmacology*; D053583:Interleukin-1beta / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D008315:Malondialdehyde / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D009205:Myocarditis / Q000378:metabolism / Q000517:prevention & control* / Q000821:virology; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D020011:Protective Agents / Q000494:pharmacology; D011897:Random Allocation; D013440:Sulfides / Q000494:pharmacology; D013482:Superoxide Dismutase / Q000378:metabolism; D051996:Transcription Factor RelA / Q000378:metabolism; D019210:Troponin I / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D053583:Interleukin-1beta; D015850:Interleukin-6; D020011:Protective Agents; D013440:Sulfides; D051996:Transcription Factor RelA; D019210:Troponin I; D014409:Tumor Necrosis Factor-alpha; D008315:Malondialdehyde; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; C025451:sodium bisulfide; D006862:Hydrogen Sulfide