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Evidence-Based Complementary and Alternative Medicine
Volume 2012, Article ID 982396, 13 pages
Research Article

Catenarin Prevents Type 1 Diabetes in Nonobese Diabetic Mice via Inhibition of Leukocyte Migration Involving the MEK6/p38 and MEK7/JNK Pathways

1Agricultural Biotechnology Research Center, Academia Sinica, 128 Academia Road, Section 2, Nankang, Taipei, Taiwan
2Institute of Basic Medical Sciences and Department of Microbiology and Immunology, National Cheng Kung University, Tainan, Taiwan
3Department of Aquaculture, National Taiwan Ocean University, Keelung 20224, Taiwan
4Department of Chinese Medicine, Buddhist Tzu Chi General Hospital, Hualien 970, Taiwan
5Institut de Génétique Humaine (CNRS UPR-1142), 141 rue de la Cardonille, 34396 Montpellier Cedex 05, France
6Department of Pharmacology, Taipei Medical University, Taipei 110, Taiwan
7Department of Veterinary Medicine, National Chung Hsing University, Taichung 402, Taiwan

Received 16 September 2011; Accepted 11 October 2011

Academic Editor: Angelo Antonio Izzo

Copyright © 2012 Ming-Yi Shen 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.


Inflammation contributes to leukocyte migration, termed insulitis, and β-cell loss in type 1 diabetes (T1D). Naturally occurring anthraquinones are claimed as anti-inflammatory compounds; however, their actions are not clear. This study aimed to investigate the effect and mechanism of catenarin on the inflammatory disease, T1D. Catenarin and/or its anthraquinone analogs dose-dependently suppressed C-X-C chemokine receptor type 4 (CXCR4)- and C-C chemokine receptor type 5 (CCR5)-implicated chemotaxis in leukocytes. Catenarin, the most potent anthraquinone tested in the study, prevented T1D in nonobese diabetic mice. Mechanistic study showed that catenarin did not act on the expression of CCR5 and CXCR4. On the contrary, catenarin inhibited CCR5- and CXCR4-mediated chemotaxis via the reduction of the phosphorylation of mitogen-activated protein kinases (p38 and JNK) and their upstream kinases (MKK6 and MKK7), and calcium mobilization. Overall, the data demonstrate the preventive effect and molecular mechanism of action of catenarin on T1D, suggesting its novel use as a prophylactic agent in T1D.