Experimental Animals
Online ISSN : 1881-7122
Print ISSN : 1341-1357
ISSN-L : 0007-5124
Original
Anti-Inflammatory Effect of Guan-Xin-Er-Hao via the Nuclear Factor-Kappa B Signaling Pathway in Rats with Acute Myocardial Infarction
Xue-Ya ZHANGXi HUANGFeng QINPing REN
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ジャーナル オープンアクセス

2010 年 59 巻 2 号 p. 207-214

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抄録
A traditional Chinese medicine, Guan-Xin-Er-Hao (GXEH), is a famous multiple target therapeutic polypharmaceutical. Our aim was to evaluate whether or not oral administration of GXEH has an anti-inflammatory effect associated with blockade of nuclear factor-kappa B (NF-κB), and to investigate the NF-κB-mediated pro-inflammatory cytokines expression pathway during acute myocardial infarction (AMI) in rats. Sprague-Dawley rats were randomly assigned to four groups: oral GXEH administered at 15 or 5 g/kg, the vehicle control and sham-operated groups. Thirty minutes after giving GXEH or 0.9% NaCl (p.o.) once, coronary arteries were occluded except for the sham-operated rats. We measured 24-h infarct size, 3-h expression of NF-κB protein in the myocardial left ventricular tissues and serum levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and C-reactive protein (CRP). Compared with rats receiving vehicle, rats administered 15 g/kg GXEH had significantly reduced 24-h infarct size, expression of NF-κB protein and serum concentrations of TNF-α, IL-6, and CRP. GXEH at 5 g/kg did not have a significant effect on these parameters. In conclusion, GXEH exhibited an anti-inflammatory effect through inhibition of the NF-κB-mediated signaling pathway leading to downregulation of pro-inflammatory cytokine expression. These findings provide new evidence of the cardioprotective effect of GXEH through reduction of infarct size by mediating lots of endogenous materials via multiple pathways to act on myocardial cells in the treatment of cardiovascular disease.
著者関連情報
© 2010 Japanese Association for Laboratory Animal Science

This article is licensed under a Creative Commons [Attribution-NonCommercial-NoDerivatives 4.0 International] license.
https://creativecommons.org/licenses/by-nc-nd/4.0/
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