Valsartan Attenuates Atherosclerosis via Upregulating the Th2 Immune Response in Prolonged Angiotensin II-Treated ApoE-/- Mice
Valsartan Attenuates Atherosclerosis via Upregulating the Th2 Immune Response in Prolonged Angiotensin II-Treated ApoE-/- Mice
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DOI：
10.2119/molmed.2014.00195
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发表时间：
2015-01-01
期刊：
影响因子：
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通讯作者：
Zhou, Yujie
中科院分区：
文献类型：
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作者：
Meng, Kai;Zeng, Qiutang;Zhou, Yujie
缬沙坦在人类和实验动物模型中对高血压和动脉粥样硬化具有保护作用。本研究旨在探讨血管紧张素II（Ang II）长期治疗对动脉粥样硬化的影响以及缬沙坦对CD 4（+）T淋巴细胞亚群活性的影响。结果显示，外源性Ang II长期干预（8周）可通过调节CD 4 + T淋巴细胞活性，包括Th 1和Th 17细胞增加，Th 2和调节性T细胞减少，导致动脉粥样硬化斑块大小增加，斑块由稳定型向不稳定型转变。相反，缬沙坦治疗有效地逆转了CD 4（+）T淋巴细胞活性的失衡，改善了动脉粥样硬化，并在控制血压的同时引起了稳定的斑块表型。此外，抗白细胞介素（IL）-5单克隆抗体治疗减弱了缬沙坦的抗动脉粥样硬化作用，而不影响血压。
Valsartan has a protective effect against hypertension and atherosclerosis in humans and experimental animal models. This study aimed to determine the effect of prolonged treatment with angiotensin II (Ang II) on atherosclerosis and the effect of valsartan on the activity of CD4(+) T lymphocyte subsets. The results showed that prolonged treatment (8 wks) with exogenous Ang II resulted in an increased atherosclerotic plaque size and a switch of stable-to-unstable plaque via modulating on CD4(+) T lymphocyte activity, including an increase in the T helper cell type 1 (Th1) and Th17 cells and a decrease in Th2 and regulatory T (Treg) cells. In contrast, valsartan treatment efficiently reversed the imbalance in CD4(+) T lymphocyte activity, ameliorated atherosclerosis and elicited a stable plaque phenotype in addition to controlling blood pressure. In addition, treatment with anti-interleukin (IL)-5 monoclonal antibodies weakened the antiatherosclerotic effects of valsartan without affecting blood pressure.