Arginase I Attenuates Inflammatory Cytokine Secretion Induced by Lipopolysaccharide in Vascular Smooth Muscle Cells
Arginase I Attenuates Inflammatory Cytokine Secretion Induced by Lipopolysaccharide in Vascular Smooth Muscle Cells
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DOI：
10.1161/atvbaha.111.229302
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发表时间：
2011-08-01
影响因子：
8.7
通讯作者：
Zhang, Ming-Xiang
中科院分区：
文献类型：
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作者：
Wang, Xu-ping;Chen, Yu-guo;Zhang, Ming-Xiang
炎症在动脉粥样硬化中起重要作用。精氨酸酶I（Arg I）促进血管平滑肌细胞的增殖;然而，Arg I对炎症的影响仍然未知。本研究探讨的作用，精氨酸我在炎症中的体外和体内。方法和结果定量逆转录聚合酶链反应和蛋白质印迹分析表明，精氨酸我抑制肿瘤坏死因子-α的生产诱导的脂多糖在人主动脉平滑肌细胞。诱导型一氧化氮合酶底物竞争和核因子-κ B激活是脂多糖介导的炎症细胞因子产生的主要因素。然而，Arg I可减弱诱导型一氧化氮合酶的功能，并抑制随后的核因子-κ B活化，从而抑制肿瘤坏死因子-α的产生。此外，上调的精氨酸我显着降低巨噬细胞浸润和炎症在兔动脉粥样硬化斑块，而下调的精氨酸我加重了这些不利影响。结论-结果表明，精氨酸的影响，并建议一个意想不到的有益作用，精氨酸我在炎症性疾病。（Arterioscler Thromb Vasc Biol.2011;31：1853-1860.）
Objective-Inflammation plays an important role in atherosclerosis. Arginase I (Arg I) promotes the proliferation of vascular smooth muscle cells; however, the effect of Arg I on inflammation remains unknown. The present study investigated the role of Arg I in inflammation in vitro and in vivo.Methods and Results-Quantitative reverse transcription-polymerase chain reaction and Western blot analysis demonstrated that Arg I inhibited tumor necrosis factor-alpha production induced by lipopolysaccharide in human aortic smooth muscle cells. Inducible nitric oxide synthase substrate competition and nuclear factor-kappa B activation were main contributors to lipopolysaccharide-mediated inflammatory cytokine generation. However, Arg I could attenuate the function of inducible nitric oxide synthase and inhibit the subsequent nuclear factor-kappa B activation, leading to inhibition of tumor necrosis factor-alpha generation. Furthermore, upregulation of Arg I significantly decreased macrophage infiltration and inflammation in atherosclerotic plaque of rabbits, whereas downregulation of Arg I aggravated these adverse effects.Conclusion-The results indicate the antiinflammatory effects of Arg I and suggest an unexpected beneficial role of Arg I in inflammatory disease. (Arterioscler Thromb Vasc Biol. 2011;31:1853-1860.)