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[Study of L-NAME treatment on experimental autoimmune myocarditis].
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2013 Mar; 29(2):119-23.ZY

Abstract

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.

Authors+Show Affiliations

The First Department of Cardiovascular Internal Medicine of South Building, Chinese PLA General Hospital, Beijing 100853, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

English Abstract
Journal Article
Research Support, Non-U.S. Gov't

Language

chi

PubMed ID

23833961

Citation

Ding, Guo-Lei, et al. "[Study of L-NAME Treatment On Experimental Autoimmune Myocarditis]." Zhongguo Ying Yong Sheng Li Xue Za Zhi = Zhongguo Yingyong Shenglixue Zazhi = Chinese Journal of Applied Physiology, vol. 29, no. 2, 2013, pp. 119-23.
Ding GL, Han LN, Wang YT, et al. [Study of L-NAME treatment on experimental autoimmune myocarditis]. Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2013;29(2):119-23.
Ding, G. L., Han, L. N., Wang, Y. T., Liu, J. W., He, S., & Zou, X. (2013). [Study of L-NAME treatment on experimental autoimmune myocarditis]. Zhongguo Ying Yong Sheng Li Xue Za Zhi = Zhongguo Yingyong Shenglixue Zazhi = Chinese Journal of Applied Physiology, 29(2), 119-23.
Ding GL, et al. [Study of L-NAME Treatment On Experimental Autoimmune Myocarditis]. Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2013;29(2):119-23. PubMed PMID: 23833961.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Study of L-NAME treatment on experimental autoimmune myocarditis]. AU - Ding,Guo-Lei, AU - Han,Li-Na, AU - Wang,Yu-Tang, AU - Liu,Jian-Wei, AU - He,Shuang, AU - Zou,Xiao, PY - 2013/7/10/entrez PY - 2013/7/10/pubmed PY - 2014/1/24/medline SP - 119 EP - 23 JF - Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology JO - Zhongguo Ying Yong Sheng Li Xue Za Zhi VL - 29 IS - 2 N2 - 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. SN - 1000-6834 UR - https://www.unboundmedicine.com/medline/citation/23833961/[Study_of_L_NAME_treatment_on_experimental_autoimmune_myocarditis]_ L2 - https://medlineplus.gov/autoimmunediseases.html DB - PRIME DP - Unbound Medicine ER -