| Budget Amount *help |
¥6,700,000 (Direct Cost: ¥6,700,000)
Fiscal Year 1993: ¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1992: ¥4,300,000 (Direct Cost: ¥4,300,000)
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| Research Abstract |
In order to investigate the pathogenesis of myocaradial injury in viral myocarditis and subsequent myocardial disorders, we measured quantitatively expression of superoxide dismutase messenger RNA in an animal model of viral myocarditis in which cDNA was synthesized by the polymerase chain reaction.4-wk-old BALB/c mice were inoculated with the encephalomyocarditis virus, and treated with captopril or N, 2-mercapto-propionyl glycine(MPG), a sulfhydryl-containing amino acid derivative without ACE inhibiting property, from days 4 to 14. On day 14, captopril and MPG significantly improved survival of mice and myocardial injury (necrosis, cellular infiltration, and calcification) in a dosedependent manner compared with the infected control group. Thus, captopril and MPG were effective for the treatment of virus-induced myocarditis. Furthermore, a striking induction of manganese superoxide dismutase (Mn-SOD) and copper / zinc SOD (Cu / ZnSOD) when compared with age-matched uninfected mice hearts. MPG completely inhibited the increase of both mRNAs, even when treatment was started on day 4. Thus, oxygen radicals may play an important role in the pathogenesis of viral myocarditis, and a therapeutic approach by eliminating oxygen radicals seems possible.
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