Role of the angiotensin II AT2 receptor in inflammation and oxidative stress: opposing effects in lean and obese Zucker rats
Role of the angiotensin II AT2 receptor in inflammation and oxidative stress: opposing effects in lean and obese Zucker rats
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DOI：
10.1152/ajprenal.00616.2010
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发表时间：
2011-03-01
影响因子：
4.2
通讯作者：
Hussain, Tahir
中科院分区：
文献类型：
--
作者：
Sabuhi, Rifat;Ali, Quaisar;Hussain, Tahir
[10] Nan R，Nan Q，Nan M，Nan R，Nan M.血管紧张素II AT 2受体在炎症和氧化应激中的作用：在瘦和肥胖Zucker大鼠中的相反作用。美国肾脏生理学杂志300：F700-F706，2011年。首次发表于2011年1月5日; doi：10.1152/ajprenal.00616.2010。炎症和氧化应激被认为有助于肥胖/糖尿病中的高血压。最近，我们报道了AT 2受体在肥胖Zucker大鼠血压控制中的作用。然而，AT 2受体在肥胖症的炎症和氧化应激中的作用尚不清楚。因此，在本研究中，我们测试了AT 2受体激动剂CGP-42112 A对肥胖Zucker大鼠炎症和氧化应激的影响，并将其与瘦大鼠进行了比较。大鼠用溶媒（对照）或CGP-42112 A（1 μ g.kg（-1）.min（-1）;渗透泵）全身处理2周。测定炎症标志物（CRP、MCP-1、TNF-α和IL-6）和氧化应激（HO-1、gp-91 phox）以及抗氧化剂（SOD）。与对照瘦大鼠相比，对照肥胖大鼠的CRP、MCP-1、TNF-α、IL-6和HO-1的血浆水平较高。相反，血浆超氧化物歧化酶活性低于对照肥胖比对照瘦大鼠。此外，TNF-α和gp-91 phox的蛋白水平在对照肥胖大鼠的肾皮质中更高。有趣的是，肥胖大鼠中的CGP-42112 A治疗降低了血浆和肾皮质炎症（TNF-α，IL-6）和氧化应激（gp-91 phox）标志物，并增加了血浆SOD活性，达到瘦对照大鼠中观察到的水平。然而，CGP-42112 A治疗瘦大鼠会增加血浆和肾皮质中的炎症（TNF-α、IL-6）和氧化应激（gp-91 phox）标志物。我们目前的研究表明，AT 2受体在肥胖Zucker大鼠中具有抗炎和抗氧化功能，而在瘦Zucker大鼠中具有促炎和促氧化功能。
Sabuhi R, Ali Q, Asghar M, Al-Zamily NR, Hussain T. Role of the angiotensin II AT2 receptor in inflammation and oxidative stress: opposing effects in lean and obese Zucker rats. Am J Physiol Renal Physiol 300: F700-F706, 2011. First published January 5, 2011; doi:10.1152/ajprenal.00616.2010.-Inflammation and oxidative stress are believed to contribute to hypertension in obesity/diabetes. Recently, we reported a role for the AT2 receptor in blood pressure control in obese Zucker rats. However, the role of AT2 receptors in inflammation and oxidative stress in obesity is not known. Therefore, in the present study, we tested the effects of the AT2 receptor agonist CGP-42112A on inflammation and oxidative stress in obese Zucker rats and compared them in their lean counterparts. Rats were systemically treated with either vehicle (control) or CGP-42112A (1 mu g.kg(-1).min(-1); osmotic pump) for 2 wk. Markers of inflammation (CRP, MCP-1, TNF-alpha, and IL-6) and oxidative stress (HO-1, gp-91phox) as well as an antioxidant (SOD) were determined. Control obese rats had higher plasma levels of CRP, MCP-1, TNF-alpha, IL-6, and HO-1 compared with control lean rats. Conversely, plasma SOD activity was lower in control obese than in control lean rats. Furthermore, the protein levels of TNF-alpha and gp-91phox were higher in the kidney cortex of control obese rats. Interestingly, CGP-42112A treatment in obese rats reduced the plasma and kidney cortex inflammatory (TNF-alpha, IL-6) and oxidative stress (gp-91phox) markers and increased plasma SOD activity to the levels seen in lean control rats. However, CGP-42112A treatment in lean rats increased inflammatory (TNF-alpha, IL-6) and oxidative stress (gp-91phox) markers in the plasma and kidney cortex. Our present studies suggest anti-inflammatory and antioxidative functions of AT2 receptor in obese Zucker rats but proinflammatory and prooxidative functions in lean Zucker rats.