血管紧张素II诱导大鼠血管平滑肌细胞产生白细胞介素-8

Zhi Wang, Lili Zhang, Baogui Sun, Qiuyan Dai
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引用次数: 1

摘要

目的白细胞介素-8(IL-8)是一种由多种细胞类型合成的典型趋化因子。先前的研究表明,血管紧张素II(Ang II)通过诱导血管平滑肌细胞(VSMCs)中的促炎细胞因子如白细胞介素-6或单核细胞趋化蛋白-1(MCP-1)参与动脉粥样硬化的形成,而Ang II对血管平滑肌细胞中IL-8表达的作用研究较少。方法从sd大鼠胸主动脉中分离VSMCs。免疫组化法证实平滑肌α-肌动蛋白的表达。采用半定量RT-PCR和酶联免疫吸附法(ELISA)检测IL-8的表达。结果在本研究中,我们发现Ang II显著提高了大鼠VSMCs中IL-8 mRNA和蛋白水平的表达,并呈剂量依赖性和时间依赖性。结论Angⅱ可能通过诱导VSMCs炎症介质参与动脉粥样硬化。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Induction of interleukin-8 production by angiotensin II in rat vascular smooth muscle cells

Objective

Interleukin-8(IL-8) represents the prototypical chemokine that is made by a wide variety of cell types. Previously studies have suggested that angiotensin II(Ang II) is involved in atherogenesis through induction of proinflammatory cytokines such as interleukin-6 or monocyte chemoattractant protein-1(MCP-1) in vascular smooth muscle cells(VSMCs), while the role of Ang II on IL-8 expression in VSMCs is poorly studied.

Methods

In this study, VSMCs were isolated from the thoracic aorta of Sprague-Dawley rats. The expression of smooth muscle α-actin was confirmed by an immunohistochemical method. Semi-quantitative RT-PCR and enzyme-linked immunosorbent assay (ELISA) analyses were conducted to detect IL-8 expression.

Results

In the present study we found that Ang II significantly increased the expression of IL-8 both at the mRNA and protein levels in rat VSMCs in a dose- and time-dependent manner.

Conclusion

These findings suggested that Ang II may participate in atherosclerosis through induction of inflammatory mediator in VSMCs.

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