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Hindawi Publishing Corporation Oxidative Medicine and Cellular Longevity Volume 2014, Article ID 148798, 10 pages /10.1155/2014/148798 Research Article Atorvastatin Represses the Angiotensin 2-Induced Oxidative Stress and Inflammatory Response in Dendritic Cells via the PI3K/Akt/Nrf 2 Pathway Yuanji Ma,1,2 Zhaoyang Chen,1,2 Yunzeng Zou,1,2 and Junbo Ge1,2 1 Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai 200032, China 2 Institute of Biomedical Science, Fudan University, 138 Yixueyuan Road, Shanghai 200032, China Correspondence should be addressed to Junbo Ge; Jbge@ Received 12 March 2014; Revised 11 June 2014; Accepted 11 June 2014; Published 3 July 2014 Academic Editor: Ryuichi Morishita Copyright 漏 2014 Yuanji Ma et al. his is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Dendritic cells (DCs), which are highly proicient antigen-presenting cells, play a complex role in both the initiation and progression of atherosclerosis. We tested the hypothesis that the anti-inlammatory and antioxidant efects of atorvastatin may be partly mediated by the phosphatidylinositol 3-kinase/protein kinase B/transcription factor nuclear factor-erythroid 2-related factor 2 (PI3K/Akt/Nrf 2) pathway via the attenuation of DC maturation, thus reducing the inlammatory and oxidative stress responses. his study showed that angiotensin 2 (Ang 2) induced the maturation of DCs, stimulated CD83, CD40, CD80, and CD86 expression, and increased the secretion of IL-12p70, IL-6, and TNF-砘? hese efects were suppressed by atorvastatin. Atorvastatin also lowered the levels of react