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普伐他汀通过调节信号转导和激活转录因子 3（STAT3）来减轻载脂蛋白 E 基因敲除小鼠的白细胞介素-6（IL-6）作用，从而预防主动脉粥样硬化。

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.

机构信息

Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, 23 Youzheng Str, Nangang District, Harbin 150001, P.R. China.

Eye hospital, The First Affiliated Hospital of Harbin Medical University, 23 Youzheng Str, Nangang District, Harbin 150001, P.R. China.

出版信息

Int J Mol Sci. 2008 Nov;9(11):2253-2264. doi: 10.3390/ijms9112253. Epub 2008 Nov 14.

DOI:10.3390/ijms9112253
PMID:19330073
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2635628/
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.

摘要

本研究旨在确定普伐他汀通过抑制白细胞介素-6（IL-6）作用来预防主动脉粥样硬化是否依赖于 STAT3 活性的调节。给予含有 1.25%胆固醇（wt/wt）的饮食的雄性载脂蛋白 E 基因敲除（apoE-/-）小鼠分为普伐他汀组（每天给予 80mg/kg 普伐他汀）和动脉粥样硬化组。八周后，普伐他汀显著预防了动脉粥样硬化病变，并降低了血清和病变中的 IL-6 水平，显著降低了病变中磷酸化 STAT3（pSTAT3）的表达，并增加了细胞因子信号转导抑制物 3（SOCS3）的表达。我们的结果表明，普伐他汀通过抑制 IL-6 作用来预防主动脉粥样硬化的作用可能部分依赖于 STAT3 活性的调节。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6d43/2635628/7b6364cb4697/ijms-9-2253f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6d43/2635628/417006454c91/ijms-9-2253f1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6d43/2635628/a0c0f9ca463d/ijms-9-2253f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6d43/2635628/7b6364cb4697/ijms-9-2253f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6d43/2635628/417006454c91/ijms-9-2253f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6d43/2635628/1774ba3f3eec/ijms-9-2253f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6d43/2635628/64f8bf1587b4/ijms-9-2253f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6d43/2635628/a0c0f9ca463d/ijms-9-2253f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6d43/2635628/7b6364cb4697/ijms-9-2253f5.jpg

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