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Published on: October 14, 2009
[Study of L-NAME treatment on experimental autoimmune myocarditis]
Guo-Lei Ding1, Li-Na Han, Yu-Tang Wang
1The First Department of Cardiovascular Internal Medicine of South Building, Chinese PLA General Hospital, Beijing 100853, China.
Objective:
To observe the therapeutic effect of N-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NOS, on experimental autoimmune myocarditis (EAM) in Balb/C mice and discuss the therapeutic mechanism induced by apoptosis.
Methods:
Thirty male Balb/C mice were divided into normal control group, model control group and experimental group randomly (n = 10). Model control group and experimental group were created into EAM by injection of porcine cardiac myosin subcutaneously in double groin and axilla and pertussis toxin intraperitoneally on day 0 and 7 respectively. Model control group was intraperitoneally administered 5 mg/(kg x day) of physiological saline after infective myosin and pertussis toxin. Experimental group was intraperitoneally given 5 mg/(kg x day) of L-NAME on day 1-21. The hearts and blood were processed after sacrificed on day 21. Cardiac inflammation score was measured by HE staining. Heart weight / body weight (HW/BW), serum nitric oxide (NO) level, activity of induced nitric oxide synthase (iNOS) and mRNA expression of iNOS in heart were measured in each group. Degree of heart apoptosis were evaluated by cardiac apoptotic index through TUNEL, immunohistochemical examination and real time PCR of Caspase-3, Caspase-8 and Caspase-9.
Results:
Compared with normal control group, cardiac inflammation score, HW/BW level of NO and activity of iNOS, mRNA expression of iNOS, the levels of mRNA and protein of Caspase-3, Caspase-8 and Caspase-9 and cardiac apoptotic index were significantly higher (P < 0.01) in model control group, and those of model control group were higher than those of experimental group (P < 0.01). HW/BW was only a little elevation in model control group compared with that in the experiment group (P < 0.05).
Conclusion:
The development of EAM is related with the NO catalyzed by iNOS. L-NAME protects cardiac myocyte via suppressing the activity of iNOS and further decreased production of NO in EAM. The mechanism might be that L-NAME alleviated myocardial inflammation through inhibited the apoptosis of cardiac myocyte.
Insights
N-nitro-L-arginine methyl ester (L-NAME) reduces inflammation and apoptosis in experimental autoimmune myocarditis (EAM) by inhibiting nitric oxide synthase (NOS). This study shows L-NAME protects cardiac myocytes in EAM.
Area of Science:
- Cardiovascular Research
- Immunology
- Pharmacology
Context:
- Experimental autoimmune myocarditis (EAM) is an inflammatory heart condition.
- Nitric oxide (NO) produced by inducible nitric oxide synthase (iNOS) plays a role in EAM pathogenesis.
- Apoptosis of cardiac myocytes contributes to myocardial damage in EAM.
Purpose:
- To evaluate the therapeutic effect of N-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase (NOS) inhibitor, on EAM in Balb/C mice.
- To investigate the mechanism of L-NAME's therapeutic action, focusing on apoptosis modulation.
Summary:
- EAM was induced in Balb/C mice, and the experimental group received L-NAME treatment.
- L-NAME administration significantly reduced cardiac inflammation, apoptosis markers (Caspase-3, -8, -9), and iNOS activity/expression compared to the model control group.
- Results indicate that L-NAME suppresses iNOS activity, decreases NO production, and alleviates myocardial inflammation by inhibiting cardiac myocyte apoptosis.
Impact:
- This study demonstrates L-NAME's protective effect against EAM in a mouse model.
- The findings suggest that targeting iNOS and subsequent apoptosis is a viable therapeutic strategy for EAM.
- L-NAME may represent a potential therapeutic agent for autoimmune myocarditis.
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