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DOCA-盐处理大鼠血管的促炎细胞因子。

Pro-inflammatory cytokines of rat vasculature in DOCA-salt treatment.

机构信息

Department of Physiology, School of Medicine, Tehran University of Medical Sciences, 14155-6447, Tehran, Iran.

出版信息

Mol Biol Rep. 2010 Apr;37(4):2111-5. doi: 10.1007/s11033-009-9676-2. Epub 2009 Aug 9.

DOI:10.1007/s11033-009-9676-2
PMID:19669669
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11708833/
Abstract

The purpose of this study was to ascertain the onset expression of pro-inflammatory cytokines in the aorta and kidney and establish their correlation with the increase in arterial blood pressure in rats subjected to DOCA-salt treatment. Male Sprague-Dawley rats underwent unilateral nephrectomy and received subcutaneous DOCA (20 mg/rat/week) as well as 1% NaCl and 0.2% KCl for drinking for 2 weeks. Blood pressure and expression of pro-inflammatory cytokines in aorta and kidney were studied weekly during the induction of hypertension. The treated rats exhibited a mild elevation of blood pressure at 1 week and a profound increase at 2 weeks. Quantitative RT-PCR demonstrated a 4.9-fold and a 3.6-fold enhancement in the expression of TNF-alpha and IL-6, respectively, in aorta as early as 1 week. The expression of IL-6 and TNF-alpha in the kidney remained almost unchanged at 1 week but mildly increased at 2 weeks DOCA-salt treatment. This study indicates a robust increase in the expression of IL-6 and TNF-alpha in aorta in DOCA-salt treated rats. This enhancement suggests that the activation of pro-inflammatory cytokines may contribute to onset of the elevation of blood pressure in DOCA-salt hypertension model.

摘要

本研究旨在确定促炎细胞因子在 DOCA-盐处理大鼠主动脉和肾脏中的起始表达,并确定其与动脉血压升高的相关性。雄性 Sprague-Dawley 大鼠接受单侧肾切除术,并接受皮下 DOCA(20mg/大鼠/周)以及 1%NaCl 和 0.2%KCl 用于饮用 2 周。在高血压诱导过程中每周研究血压和主动脉及肾脏中促炎细胞因子的表达。在 1 周时,治疗大鼠的血压出现轻度升高,在 2 周时出现明显升高。定量 RT-PCR 显示,TNF-α和 IL-6 的表达分别在 1 周时增加了 4.9 倍和 3.6 倍。在 1 周 DOCA-盐处理时,肾脏中 IL-6 和 TNF-α的表达几乎不变,但在 2 周时略有增加。本研究表明,DOCA-盐处理大鼠主动脉中 IL-6 和 TNF-α的表达显著增加。这种增强表明,促炎细胞因子的激活可能导致 DOCA-盐高血压模型中血压升高的开始。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b308/11708833/bd249cd3196d/nihms-2041144-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b308/11708833/b54f61d21cfc/nihms-2041144-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b308/11708833/bd249cd3196d/nihms-2041144-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b308/11708833/b54f61d21cfc/nihms-2041144-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b308/11708833/bd249cd3196d/nihms-2041144-f0002.jpg

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Hypertens Res. 2008 Mar;31(3):515-23. doi: 10.1291/hypres.31.515.
2
Role of the T cell in the genesis of angiotensin II induced hypertension and vascular dysfunction.T细胞在血管紧张素II诱导的高血压和血管功能障碍发生中的作用。
J Exp Med. 2007 Oct 1;204(10):2449-60. doi: 10.1084/jem.20070657. Epub 2007 Sep 17.
3
Classic interleukin-6 receptor signaling and interleukin-6 trans-signaling differentially control angiotensin II-dependent hypertension, cardiac signal transducer and activator of transcription-3 activation, and vascular hypertrophy in vivo.
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Int J Appl Basic Med Res. 2015 Jan-Apr;5(1):12-7. doi: 10.4103/2229-516X.149222.
4
Brain angiotensin-converting enzyme type 2 shedding contributes to the development of neurogenic hypertension.脑血管紧张素转化酶 2 的脱落有助于神经源性高血压的发展。
Circ Res. 2013 Oct 12;113(9):1087-1096. doi: 10.1161/CIRCRESAHA.113.301811. Epub 2013 Sep 6.
5
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PPAR Res. 2011;2011:502631. doi: 10.1155/2011/502631. Epub 2011 Dec 7.
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Hypertension. 2006 Mar;47(3):557-62. doi: 10.1161/01.HYP.0000198545.01860.90. Epub 2006 Jan 16.
7
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J Pharmacol Exp Ther. 2005 Oct;315(1):51-7. doi: 10.1124/jpet.105.088062. Epub 2005 Jun 10.
8
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J Hum Hypertens. 2005 Jun;19(6):457-62. doi: 10.1038/sj.jhh.1001845.
9
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10
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J Hypertens. 2004 May;22(5):1007-15. doi: 10.1097/00004872-200405000-00024.