Peroxisome Proliferator Activated Receptor-α Agonist Slows the Progression of Hypertension, Attenuates Plasma Interleukin-6 Levels and Renal Inflammatory Markers in Angiotensin II Infused Mice.
Peroxisome Proliferator Activated Receptor-α Agonist Slows the Progression of Hypertension, Attenuates Plasma Interleukin-6 Levels and Renal Inflammatory Markers in Angiotensin II Infused Mice.
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DOI：
10.1155/2012/645969
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发表时间：
2012
期刊：
影响因子：
2.9
通讯作者：
Lee DL
中科院分区：
文献类型：
--
作者：
Wilson JL;Duan R;El-Marakby A;Alhashim A;Lee DL
PPAR-α 的抗炎特性在减轻高血压方面发挥着重要作用。目前的研究确定了 PPAR-α 激动剂在 Ang II 缓慢升压剂量（400ng/kg/min）期间的抗高血压和抗炎作用。将遥测装置植入 10 至 12 周龄的雄性 PPAR-α KO 小鼠及其 WT 对照小鼠中，并注射 Ang II 12 天。在 Ang II 输注第 12 天，与 WT 小鼠相比，PPAR-α KO 小鼠的 MAP 升高（161 ± 4mmHg 对比 145 ± 4mmHg），非诺贝特（145mg/kg/天）降低了 WT + Ang II 小鼠的 MAP（134 ± 7mmHg）。在 Ang II 输注第 12 天，PPAR-α KO 小鼠的血浆 IL-6 水平较高（30 ± 4 vs 8 ± 2 pg/mL），非诺贝特降低了 Ang II 处理的 WT 小鼠的血浆 IL-6（10 ± 3 pg/mL）。非诺贝特增加 WT + Ang II 小鼠肾 CYP4A 表达，恢复肾 CYP2J 表达，降低肾 ICAM-1、MCP-1 和 COX-2 升高。我们的结果表明，PPAR-α 的激活通过上调 CYP4A 和 CYP2J 以及减弱炎症标志物（如血浆 IL-6、肾 MCP-1、ICAM-1 和 COX-2 的肾表达）来减轻 Ang II 诱导的高血压。
The anti-inflammatory properties of PPAR-α plays an important role in attenuating hypertension. The current study determines the anti-hypertensive and anti-inflammatory role of PPAR-α agonist during a slow-pressor dose of Ang II (400 ng/kg/min). Ten to twelve week old male PPAR-α KO mice and their WT controls were implanted with telemetry devices and infused with Ang II for 12 days. On day 12 of Ang II infusion, MAP was elevated in PPAR-α KO mice compared to WT (161 ± 4 mmHg versus 145 ± 4 mmHg) and fenofibrate (145 mg/kg/day) reduced MAP in WT + Ang II mice (134 ± 7 mmHg). Plasma IL-6 levels were higher in PPAR-α KO mice on day 12 of Ang II infusion (30 ± 4 versus 8 ± 2 pg/mL) and fenofibrate reduced plasma IL-6 in Ang II-treated WT mice (10 ± 3 pg/mL). Fenofibrate increased renal expression of CYP4A, restored renal CYP2J expression, reduced the elevation in renal ICAM-1, MCP-1 and COX-2 in WT + Ang II mice. Our results demonstrate that activation of PPAR-α attenuates Ang II-induced hypertension through up-regulation of CYP4A and CYP2J and an attenuation of inflammatory markers such as plasma IL-6, renal MCP-1, renal expression of ICAM-1 and COX-2.
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影响因子：
8.3
作者：
Vera, T;Taylor, M;Stec, DE
通讯作者：
Stec, DE
影响因子：
4
作者：
Delerive, P;Fruchart, JC;Staels, B
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影响因子：
64.8
作者：
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通讯作者：
GREEN, S
影响因子：
8.3
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Pollock, DM
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作者：
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