title: Cardioprotection of H2S by downregulating iNOS and upregulating HO-1 expression in mice with CVB3-induced myocarditis.
abstract: OBJECTIVE
  To explore the effects and potential mechanisms of hydrogen sulfide (H2S) in CVB3-induced mice with myocarditis.
  
  
  METHODS
  A total of 75 six-week-old inbred male Balb/c mice were divided randomly into four groups (N, C, P and S). Group N was the negative control. The others were inoculated intraperitoneally (i.p.) with CVB3. Subsequently, groups P and S were injected i.p. once a day with DL-Proparglygylcine (PAG) and NaHS respectively. Group C was the positive control. Inducible nitric oxide synthase (iNOS) and heme oxygenase-1(HO-1) expression on cardiac tissues were evaluated by histopathological examination, immunohistochemistry, RT-PCR and Western blot.
  
  
  RESULTS
  The heart-weight to body-weight (HW/BW) ratio, the histologic scores and the iNOS mRNA and protein expression levels were higher, and the HO-1 mRNA and protein expression levels were lower in mice treated with PAG than those mice solely inoculated with CVB3. Mice in group S had a significant decreased in the HW/BW ratio, the histologic scores and the iNOS mRNA and protein expression levels, and had a significant increased in the HO-1 mRNA and protein expression levels compared to the mice in group C. H2S can attenuate inflammatory cell infiltration, alleviate cardiac edema, and limit myocardial lesions.
  
  
  CONCLUSIONS
  Our data support that H2S can inhibit iNOS overexpression and induce HO-1 expression, both of which contribute to the cardioprotection of H2S in CVB3-induced mice myocarditis.
authors.affiliation: Department of Cardiology, Children's Hospital, Zhejiang University School of Medicine, PR China; The Key Laboratory of Reproductive Genetics (Zhejiang University), Ministry of Education, PR China.
authors.forename: Wang
authors.initials: W
authors.lastname: Hua
authors.forename: Qi
authors.initials: Q
authors.lastname: Chen
authors.forename: Fangqi
authors.initials: F
authors.lastname: Gong
authors.forename: Chunhong
authors.initials: C
authors.lastname: Xie
authors.forename: Shulai
authors.initials: S
authors.lastname: Zhou
authors.forename: Lichao
authors.initials: L
authors.lastname: Gao
mesh_terms: D000818:Animals; D015153:Blotting, Western; D003384:Coxsackievirus Infections / Q000150:complications*; D029822:Enterovirus B, Human; D051547:Heme Oxygenase-1 / Q000096:biosynthesis*; D006862:Hydrogen Sulfide / Q000494:pharmacology*; D007150:Immunohistochemistry; D007202:Indicators and Reagents; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009205:Myocarditis / Q000209:etiology* / Q000517:prevention & control*; D009206:Myocardium / Q000473:pathology; D052247:Nitric Oxide Synthase Type II / Q000096:biosynthesis*; D009929:Organ Size / Q000187:drug effects; D020011:Protective Agents; D012333:RNA, Messenger / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D015996:Survival Rate
chemical_list: D007202:Indicators and Reagents; D020011:Protective Agents; D012333:RNA, Messenger; D052247:Nitric Oxide Synthase Type II; D051547:Heme Oxygenase-1; D006862:Hydrogen Sulfide
keywords: Coxsackievirus B3; Heme oxygenase-1; Hydrogen sulfide; Inducible nitric oxide synthase; Myocarditis