Tohoku J. Exp. Med., 2012, 227(3)

Emodin, a Naturally Occurring Anthraquinone, Ameliorates Experimental Autoimmune Myocarditis in Rats

ZHAN-CHUN SONG,^1,2 ZHAN-SHENG WANG,¹ JING-HUI BAI,^1,3 ZHAO LI¹ and JIAN HU¹

¹Department of Cardiology, The First Hospital of China Medical University, China Medical University, Shenyang, P.R. China
²Department of Cardiology, Fushun Central Hospital, Fushun, P.R. China
³Intensive care unit, Liaoning Cancer Hospital, Shenyang, P.R. China

Myocarditis is an inflammatory disease of the heart and a major cause of dilated cardiomyopathy that can lead to heart failure and sudden death in young adults. Giant cell myocarditis is a severe heart disease of unknown causes and is defined histopathologically as diffuse myocardial necrosis with multinucleated giant cells in the absence of sarcoid-like granulomata. Giant cell myocarditis is often studied using a model of experimental autoimmune myocarditis (EAM) in rats. Emodin is an important component of traditional Chinese herb rhubarb, and has well-documented anti-inflammatory effect. The current study determined the potential efficacy of emodin using a rat model of EAM. Male Lewis rats (6 weeks of age) were immunized on days 0 and 7 with a porcine cardiac myosin at both footpads to induce EAM. Simultaneously with the immunization, rats received emodin (50 mg/kg/day) or distilled water by intragastric administration for 3 weeks (8 animals/group). Likewise, eight animals were immunized with adjuvant alone and treated with distilled water. The immunization significantly enlarged the hearts due to inflammatory lesions. Emodin treatment significantly improved left ventricular (LV) function and reduced the severity of myocarditis, as reflected by echocardiographic and histopathological examination. Emodin treatment decreased the serum levels of proinflammatory cytokines tumor necrosis factor (TNF)-α and interleukin (IL)-1β. Nuclear factor-κBp65 (NF-κBp65), a rapid-response transcription factor that regulates proinflammatory cytokines, in the myocardial tissue was also suppressed in the treated rats. In conclusion, emodin could ameliorate EAM, at least in part, by decreasing the production of proinflammatory cytokines TNF-α and IL-1β.

keywords —— emodin; experimental autoimmune myocarditis; heart failure; inflammation; myocarditis

© 2012 Tohoku University Medical Press

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Tohoku J. Exp. Med., 2012, 227, 225-230