Quercetin offers cardioprotection against progression of experimental autoimmune myocarditis by suppression of oxidative and endoplasmic reticulum stress via endothelin-1/MAPK signalling

Somasundaram Arumugam, Rajarajan A. Thandavarayan, Wawaimuli Arozal, Flori R. Sari, Vijayasree V. Giridharan, Vivian Soetikno, Suresh S. Palaniyandi, Meilei Harima, Kenji Suzuki, Masaki Nagata, Ritsuo Tagaki, Makoto Kodama, Kenichi Watanabe

Research output: Contribution to journalArticlepeer-review

51 Scopus citations

Abstract

In order to test the hypothesis that treatment with quercetin at a dose of 10 mg/kg protects from the progression of experimental autoimmune myocarditis (EAM) to dilated cardiomyopathy (DCM), we have used the rat model of EAM induced by porcine cardiac myosin. Our results identified that the post-myocarditis rats suffered from elevated endoplasmic reticulum (ER) stress and adverse cardiac remodelling in the form of myocardial fibrosis, whereas the rats treated with quercetin have been protected from these changes as evidenced by the decreased myocardial levels of ER stress and fibrosis markers when compared with the vehicle-treated DCM rats. In addition, the myocardial dimensions and cardiac function were preserved significantly in the quercetin-treated rats in comparison with the DCM rats treated with vehicle alone. Interestingly, the rats treated with quercetin showed significant suppression of the myocardial endothelin-1 and also the mitogen activated protein kinases (MAPK) suggesting that the protection offered by quercetin treatment against progression of EAM involves the modulation of MAPK signalling cascade. Collectively, the present study provides data to support the role of quercetin in protecting the hearts of the rats with post myocarditis DCM.

Original languageEnglish (US)
Pages (from-to)154-163
Number of pages10
JournalFree Radical Research
Volume46
Issue number2
DOIs
StatePublished - Feb 2012

Keywords

  • adverse cardiac remodelling
  • apoptosis
  • fibrosis
  • mitogen activated protein kinase signalling
  • oxidative stress

ASJC Scopus subject areas

  • Biochemistry

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