Artemisinin Attenuates Post-Infarct Myocardial Remodeling by Down-Regulating the NF-κB Pathway

Jun 26, 2012The Tohoku journal of experimental medicine

Artemisinin reduces heart muscle changes after a heart attack by lowering NF-κB pathway activity

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Abstract

The artemisinin-treated group showed a survival rate of 65% compared to 40% in the vehicle-treated group four weeks after myocardial infarction.

Artemisinin may improve cardiac function and left ventricular dimensions following myocardial infarction.
Both groups had similar infarct sizes, suggesting that artemisinin's benefits are independent of the extent of heart muscle damage.
Myocardial fibrosis and levels of fibrosis-related factors were significantly reduced in the artemisinin-treated group.
Artemisinin is associated with the inhibition of the NF-κB pathway by blocking specific protein phosphorylation.

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Myocardial infarction (MI) leads to progressive left ventricular (LV) dilatation and is associated with interstitial fibrosis in the non-infarcted myocardium. The NF-κB signaling pathway plays an important role in ventricular remodeling after MI. Recent studies have indicated that the anti-malarial agent artemisinin can inhibit NF-κB activation, which may attenuate post-infarct myocardial remodeling. In this study, we investigated the effect of artemisinin on post-infarct myocardial remodeling using a rat model of MI. Adult male Sprague Dawley rats were divided into a sham group (n = 10) and MI groups that were treated either with oral gavage of artemisinin (75 mg/kg/day, n = 20) or vehicle (0.5% carboxymethyl cellulose, n = 20) three times a day for 4 weeks. Each treatment was started at 24 hours after ligation of the left anterior descending coronary artery. Four weeks after MI, the artemisinin-treated group showed a significantly improved survival rate compared with that of the vehicle-treated group (65% vs. 40%, P < 0.05). Although infarct size was similar in both groups, echocardiography showed significant improvements in cardiac function and left ventricular dimensions in the artemisinin-treated group. Moreover, the degree of myocardial fibrosis and elevated levels of fibrosis-related factors [transforming growth factor-β1, collagen type I, matrix metalloproteinase (MMP)-2 and MMP-9] in the non-infarcted myocardium were remarkably ameliorated by artemisinin (all P < 0.05). Importantly, artemisinin inhibited the NF-κB pathway by blocking IKBα phosphorylation. In conclusion, artemisinin may attenuate post-infarct myocardial remodeling by down-regulating the NF-κB pathway.

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Artemisinin Attenuates Post-Infarct Myocardial Remodeling by Down-Regulating the NF-κB Pathway

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