Wild Panax Ginseng (Panax ginseng C.A. Meyer) Protects Against Methotrexate–Induced Cell Regression by Enhancing the Immune Response in RAW 264.7 Macrophages

2010 ◽  
Vol 38 (05) ◽  
pp. 949-960 ◽  
Author(s):  
Hyo Il Jang ◽  
Heung Mook Shin

Many traditional herbal medicines have been re-evaluated to determine whether they enhance immune responses. In this study, the possible use of wild Panax ginseng (WPG) for enhancement of host immunity in chemotherapy was investigated. In the cell proliferation assay, WPG significantly enhanced the proliferation of RAW 264.7 macrophages and protected against cell regression in macrophages treated with methotrexate (MTX). WPG induced the production of nitric oxide and the expression of inducible nitric oxide synthase and cyclooxygense-2 mRNA. Furthermore, WPG enhanced the production of cytokines including interleukin (IL)-1α, IL-1β, IL-6, tumor necrosis factor-α and granulocyte-macrophage colony-stimulating factor, and chemokines such as macrophage chemotactic protein-1 and regulated upon activation, normal T-cell expressed and secreted (RANTES), regardless of MTX co-administration. Taken together, these results provide the first evidence that WPG triggers immune responses through the prevention of macrophage cell regression caused by MTX and functional activation of macrophages.

Blood ◽  
2006 ◽  
Vol 109 (7) ◽  
pp. 3084-3087 ◽  
Author(s):  
Lars C. Jacobsen ◽  
Kim Theilgaard-Mönch ◽  
Erik I. Christensen ◽  
Niels Borregaard

Abstract Arginase 1 (ARG1) metabolizes arginine, thus reducing the availability of arginine as a substrate for nitric oxide synthase (NOS). The decreased production of nitric oxide (NO) by NOS and the production of ornithine by ARG1 affect immune responses and tissue regeneration at sites of infection, respectively. We here demonstrate that ARG1 is synthesized in myelocytes/metamyelocytes and is stored in gelatinase granules. In accordance with this, activated neutrophils coreleased ARG1 and gelatinase to the extracellular environment on stimulation with phorbol-12-myristate 13-acetate (PMA), formyl-methionyl-leucyl-phenylalanine (fMLP), or tumor necrosis factor α (TNF-α). Overall, these findings define ARG1 as a genuine gelatinase granule protein and support a model in which activated neutrophils release ARG1 at sites of infection to modulate immune responses and promote tissue regeneration.


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