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Mediators of Inflammation
Volume 2017, Article ID 5706152, 14 pages
Research Article

Aloperine Protects Mice against DSS-Induced Colitis by PP2A-Mediated PI3K/Akt/mTOR Signaling Suppression

1Department of Clinical Immunology, Institute of Laboratory Medicine, Guangdong Medical University, No. 1 Xincheng Road, Dongguan 523808, China
2The Center for Biomedical Research, Key Laboratory of Organ Transplantation, Ministry of Education, Tongji Hospital, Huazhong University of Science and Technology, Wuhan 430030, China
3Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics, No. 1 Xincheng Road, Dongguan 523808, China
4Cardiovascular Research Institute, Case Western Reserve University, 2103 Cornell Road, Cleveland, OH 44106, USA
5Mathematical Engineering Academy of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou 510006, China

Correspondence should be addressed to Xuebao Zheng; moc.anis@gnehzoabeux and Jun-Fa Xu; nc.ude.umdg@afnujux

Received 17 April 2017; Revised 27 June 2017; Accepted 30 July 2017; Published 19 September 2017

Academic Editor: Julio Galvez

Copyright © 2017 Xiaoxia Fu et al. This 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.


Colitis is a major form of inflammatory bowel disease which involved mucosal immune dysfunction. Aloperine is an alkaloid isolated from the shrub Sophora alopecuroides L. and has been recognized as an effective treatment for inflammatory and allergic diseases. The present study aimed to examine the molecular mechanisms underlying aloperine-mediated colitis protection. We found that aloperine treatment improved colitis induced by dextran sodium sulfate (DSS) based on body weight, disease activity index, colonic length, and spleen index. Aloperine also effectively attenuated DSS-induced intestinal inflammation based on the pathological score and myeloperoxidase expression and activity in colon tissues. In addition, aloperine regulated T-cell proportions and promoted Foxp3 expression in the spleens and mesenteric lymph nodes of DSS-induced colitis mice and in the spleens of the Foxp3GFP mice. Aloperine inhibited Jurkat and mouse naïve T-cell apoptosis. Furthermore, aloperine inhibited PI3K/Akt/mTOR signaling and upregulated PP2A expression in the DSS-induced colitis mice and in Jurkat cells, but LB-100 (PP2A inhibitor) resulted in an elevated Akt activity in Jurkat cells, activated T-cells, and human splenic mononuclear cells. Aloperine inhibited T-cell and lymphocyte proliferation, but LB-100 reverse these effects. In conclusion, aloperine regulates inflammatory responses in colitis by inhibiting the PI3K/Akt/mTOR signaling in a PP2A-dependent manner.