Catenarin prevents type 1 diabetes in nonobese diabetic mice via inhibition of leukocyte migration involving the MEK6/p38 and MEK7/JNK pathways

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

doi:10.1155/2012/982396

Catenarin prevents type 1 diabetes in nonobese diabetic mice via inhibition of leukocyte migration involving the MEK6/p38 and MEK7/JNK pathways

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

Research output: Contribution to journal › Article › peer-review

13 Citations (Scopus)

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.

Original language	English
Article number	982396
Journal	Evidence-based Complementary and Alternative Medicine
Volume	2012
DOIs	https://doi.org/10.1155/2012/982396
Publication status	Published - 2012

ASJC Scopus subject areas

Complementary and alternative medicine

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1155/2012/982396

Cite this

Shen, M. Y., Lin, Y. P., Yang, B. C., Jang, Y. S., Chiang, C. K., Mettling, C., Chen, Z. W., Sheu, J. R., Chang, C. L., Lin, Y. L., & Yang, W. C. (2012). Catenarin prevents type 1 diabetes in nonobese diabetic mice via inhibition of leukocyte migration involving the MEK6/p38 and MEK7/JNK pathways. Evidence-based Complementary and Alternative Medicine, 2012, [982396]. https://doi.org/10.1155/2012/982396

Shen, MY, Lin, YP, Yang, BC, Jang, YS, Chiang, CK, Mettling, C, Chen, ZW, Sheu, JR, Chang, CL, Lin, YL & Yang, WC 2012, 'Catenarin prevents type 1 diabetes in nonobese diabetic mice via inhibition of leukocyte migration involving the MEK6/p38 and MEK7/JNK pathways', Evidence-based Complementary and Alternative Medicine, vol. 2012, 982396. https://doi.org/10.1155/2012/982396

@article{999ae7510eb1411da99b1660e78a9ed8,

title = "Catenarin prevents type 1 diabetes in nonobese diabetic mice via inhibition of leukocyte migration involving the MEK6/p38 and MEK7/JNK pathways",

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.",

author = "Shen, {Ming Yi} and Lin, {Yu Ping} and Yang, {Bei Chang} and Jang, {Yu Song} and Chiang, {Chih Kang} and Cl{\'e}ment Mettling and Chen, {Zeng Weng} and Sheu, {Joen Rong} and Chang, {Cicero L.} and Lin, {Yea Lih} and Yang, {Wen Chin}",

year = "2012",

doi = "10.1155/2012/982396",

language = "English",

volume = "2012",

journal = "Evidence-based Complementary and Alternative Medicine",

issn = "1741-427X",

publisher = "Hindawi Publishing Corporation",

}

TY - JOUR

T1 - Catenarin prevents type 1 diabetes in nonobese diabetic mice via inhibition of leukocyte migration involving the MEK6/p38 and MEK7/JNK pathways

AU - Shen, Ming Yi

AU - Lin, Yu Ping

AU - Yang, Bei Chang

AU - Jang, Yu Song

AU - Chiang, Chih Kang

AU - Mettling, Clément

AU - Chen, Zeng Weng

AU - Sheu, Joen Rong

AU - Chang, Cicero L.

AU - Lin, Yea Lih

AU - Yang, Wen Chin

PY - 2012

Y1 - 2012

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=84863268602&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84863268602&partnerID=8YFLogxK

U2 - 10.1155/2012/982396

DO - 10.1155/2012/982396

M3 - Article

C2 - 22454693

AN - SCOPUS:84863268602

SN - 1741-427X

VL - 2012

JO - Evidence-based Complementary and Alternative Medicine

JF - Evidence-based Complementary and Alternative Medicine

M1 - 982396

ER -

Catenarin prevents type 1 diabetes in nonobese diabetic mice via inhibition of leukocyte migration involving the MEK6/p38 and MEK7/JNK pathways

Abstract

ASJC Scopus subject areas

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this