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Int. J. Mol. Sci. 2008, 9(11), 2253-2264; https://doi.org/10.3390/ijms9112253

Pravastatin Prevents Aortic Atherosclerosis via Modulation of Signal Transduction and Activation of Transcription 3 (STAT3) to Attenuate Interleukin-6 (IL-6) Action in ApoE Knockout Mice

1
Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, 23 Youzheng Str, Nangang District, Harbin 150001, P.R. China
2
Eye hospital, The First Affiliated Hospital of Harbin Medical University, 23 Youzheng Str, Nangang District, Harbin 150001, P.R. China
*
Author to whom correspondence should be addressed.
Received: 27 September 2008 / Revised: 4 November 2008 / Accepted: 7 November 2008 / Published: 14 November 2008
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
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Abstract

The purpose of this study was to determine whether pravastatin’s prevention of aortic atherosclerosis via attenuation of IL-6 action depends on modulation of STAT3 activity. Male apoE knockout (apoE-/-) mice fed on a diet containing 1.25% cholesterol (wt/wt) were divided into pravastatin group provided with pravastatin (80 mg kg-1 per day) and atherosclerosis group. After eight weeks, pravastatin significantly prevented atherosclerotic lesion and reduced levels of IL-6 in serum and lesion, and significantly decreased expressions of phosphorylated STAT3 (pSTAT3) and increased suppressor of cytokine signaling 3 (SOCS3) expressions in lesions. Our results suggested that pravastatin’s aortic atherosclerosis preventing action via attenuation of IL-6 action may partially depend on modulation of STAT3 activity. View Full-Text
Keywords: Pravastatin; atherosclerosis; IL-6; STAT3; SOCS3 Pravastatin; atherosclerosis; IL-6; STAT3; SOCS3
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).
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Zhou, X.; Li, D.; Yan, W.; Li, W. Pravastatin Prevents Aortic Atherosclerosis via Modulation of Signal Transduction and Activation of Transcription 3 (STAT3) to Attenuate Interleukin-6 (IL-6) Action in ApoE Knockout Mice. Int. J. Mol. Sci. 2008, 9, 2253-2264.

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