Inhibition of endogenous hydrogen sulfide production improves viral elimination in CVB3-infected myocardium in mice.

ABSTRACT

BACKGROUND: To find whether administration of hydrogen sulfide has interaction with coxsackie virus B3 (CVB3) replication and spread. METHODS: Six-week-old inbred male Balb/c mice were injected intraperitoneally with CVB3. Mice were randomized to four groups (n = 10 for each group) group N (sham infection + vehicle), group C (virus + vehicle), group P (virus + DL-proparglygylcine (PAG)), and group S (virus + sodium hydrogen sulfide (NaHS)). PAG and NaHS were administered intraperitoneally daily and mice were killed on day 4 after viral inoculation. Serum specimens were obtained to assay tumor necrosis factor-α (TNFα) level, and heart specimens were harvested for histological examination, 50% tissue culture infection dose (TCID50) assay, reverse transcription-polymerase chain reaction and Western blot analysis. RESULTS: The ratio of heart-weight to body-weight and inflammatory scores showed no significant difference between infected groups. The circulatory and local concentrations of TNFα, nitric oxide synthase 2 messenger RNA, and protein were higher in group P, and were lower in group S compared to those in group C. Mice treated with PAG and NaHS had significantly lower and higher viral stocks than those inoculated with CVB3 only, respectively. CONCLUSION: Inhibition of endogenous hydrogen sulfide production contributed to viral clearance in acute viremia of CVB3-induced myocarditis.