Next Article in Journal
CO2 Adsorption on Activated Carbon Honeycomb-Monoliths: A Comparison of Langmuir and Tóth Models
Previous Article in Journal
Risk-Association of DNA Methyltransferases Polymorphisms with Gastric Cancer in the Southern Chinese Population
Int. J. Mol. Sci. 2012, 13(7), 8379-8387; doi:10.3390/ijms13078379
Article

Astragalus membranaceus Inhibits Inflammation via Phospho-P38 Mitogen-Activated Protein Kinase (MAPK) and Nuclear Factor (NF)-κB Pathways in Advanced Glycation End Product-Stimulated Macrophages

1
,
1
,
2
,
2
,
2
 and
1,3,*
Received: 25 April 2012 / Revised: 22 June 2012 / Accepted: 29 June 2012 / Published: 5 July 2012
View Full-Text   |   Download PDF [376 KB, uploaded 19 June 2014]   |   Browse Figures

Abstract

Advanced glycation end products (AGEs) and inflammation contribute to the development of diabetic complications. Astragalus membranaceus has properties of immunological regulation in many diseases. The aim of this study was to determine the function of A. membranaceus extract (AME) on the AGE-induced inflammatory response in Ana-1 macrophages. The viability of cells treated with AME or AGEs was evaluated with the MTT [3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide] method. The secretion and mRNA levels of IL-1β and TNF-α were measured by ELISA and RT-PCR, respectively. The activity of NF-κB was assayed by EMSA. The phosphorylation of p38 MAPK was assessed by western blotting. The results showed that AME was not toxic to macrophages. The treatment of macrophages with AME effectively inhibited AGE-induced IL-1β and TNF-α secretion and mRNA expression in macrophages. These effects may be mediated by p38 MAPK and the NF-κB pathway. The results suggest that AME can inhibit AGE-induced inflammatory cytokine production to down-regulate macrophage-mediated inflammation via p38 MAPK and NF-κB signaling pathways and indicate that AME could be an immunoregulatory agent against AGE-induced inflammation in diabetes.
Keywords: Astragalus membranaceus; advanced glycation end products; macrophage; inflammation; diabetes Astragalus membranaceus; advanced glycation end products; macrophage; inflammation; diabetes
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.

Share & Cite This Article

Further Mendeley | CiteULike
Export to BibTeX |
EndNote
MDPI and ACS Style

Qin, Q.; Niu, J.; Wang, Z.; Xu, W.; Qiao, Z.; Gu, Y. Astragalus membranaceus Inhibits Inflammation via Phospho-P38 Mitogen-Activated Protein Kinase (MAPK) and Nuclear Factor (NF)-κB Pathways in Advanced Glycation End Product-Stimulated Macrophages. Int. J. Mol. Sci. 2012, 13, 8379-8387.

View more citation formats

Related Articles

Article Metrics

For more information on the journal, click here

Comments

Cited By

[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert