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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
Department of Nephrology, Shanghai Fifth People’s Hospital, Fudan University, Shanghai 200240, China
2
School of Life Science and Biotechnology, Shanghai Jiaotong University, Shanghai 200240, China
3
Department of Nephrology, Huashan Hospital, Fudan University, Shanghai 200240, China
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2012, 13(7), 8379-8387; https://doi.org/10.3390/ijms13078379
Received: 25 April 2012 / Revised: 22 June 2012 / Accepted: 29 June 2012 / Published: 5 July 2012
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. View Full-Text
Keywords: Astragalus membranaceus; advanced glycation end products; macrophage; inflammation; diabetes Astragalus membranaceus; advanced glycation end products; macrophage; inflammation; diabetes
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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. https://doi.org/10.3390/ijms13078379

AMA 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. International Journal of Molecular Sciences. 2012; 13(7):8379-8387. https://doi.org/10.3390/ijms13078379

Chicago/Turabian Style

Qin, Qiaojing; Niu, Jianying; Wang, Zhaoxia; Xu, Wangjie; Qiao, Zhongdong; Gu, Yong. 2012. "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. 13, no. 7: 8379-8387. https://doi.org/10.3390/ijms13078379

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