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

To find whether administration of hydrogen sulfide has interaction with coxsackie virus B3 (CVB3) replication and spread.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.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.Inhibition of endogenous hydrogen sulfide production contributed to viral clearance in acute viremia of CVB3-induced myocarditis.