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Please use this identifier to cite or link to this item: http://ntour.ntou.edu.tw:8080/ir/handle/987654321/45441

Title: Catenarin prevents type 1 diabetes in non-obese diabetic mice via inhibition of leukocyte migration involving the MEK6/p38 and MEK7/JNK pathways.
Authors: Ming-Yi Shen;Yu-Ping Lin;Bei-Chang Yang;Yu-Song Jang;Chih-Kang Chiang;Clément Mettling;Zeng-Weng Chen;Joen-Rong Sheu;Cicero L. Chang;Yea-Lih Lin;Wen-Chin Yang
Contributors: 國立臺灣海洋大學:水產養殖學系
Date: 2012
Issue Date: 2018-03-19T06:22:58Z
Publisher: Complementary and Alternative Medicine
Abstract: Abstract: 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.
Relation: 2012
URI: http://ntour.ntou.edu.tw:8080/ir/handle/987654321/45441
Appears in Collections:[水產養殖學系] 期刊論文

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