10.3389/fimmu.2019.00155.s002
Dolores Limongi
Dolores
Limongi
Sara Baldelli
Sara
Baldelli
Paola Checconi
Paola
Checconi
Mariaelena Marcocci
Mariaelena
Marcocci
Giovanna De Chiara
Giovanna
De Chiara
Alessandra Fraternale
Alessandra
Fraternale
Mauro Magnani
Mauro
Magnani
Maria Rosa Ciriolo
Maria Rosa
Ciriolo
Anna Teresa Palamara
Anna Teresa
Palamara
Image_2_GSH-C4 Acts as Anti-inflammatory Drug in Different Models of Canonical and Cell Autonomous Inflammation Through NFκB Inhibition.tif
Frontiers
2019
glutathione
macrophage
adipocytes
myocytes
cytokine
2019-02-06 04:10:08
Figure
https://frontiersin.figshare.com/articles/figure/Image_2_GSH-C4_Acts_as_Anti-inflammatory_Drug_in_Different_Models_of_Canonical_and_Cell_Autonomous_Inflammation_Through_NF_B_Inhibition_tif/7678901
<p>An imbalance in GSH/GSSG ratio represents a triggering event in pro-inflammatory cytokine production and inflammatory response. However, the molecular mechanism(s) through which GSH regulates macrophage and cell autonomous inflammation remains not deeply understood. Here, we investigated the effects of a derivative of GSH, the N-butanoyl glutathione (GSH-C4), a cell permeable compound, on lipopolisaccharide (LPS)-stimulated murine RAW 264.7 macrophages, and human macrophages. LPS alone induces a significant production of pro-inflammatory cytokines, such as IL-1β, IL-6, and TNF-α and a significant decrement of GSH content. Such events were significantly abrogated by treatment with GSH-C4. Moreover, GSH-C4 was highly efficient in buffering cell autonomous inflammatory status of aged C2C12 myotubes and 3T3-L1 adipocytes by suppressing the production of pro-inflammatory cytokines. We found that inflammation was paralleled by a strong induction of the phosphorylated form of NFκB, which translocates into the nucleus; a process that was also efficiently inhibited by the treatment with GSH-C4. Overall, the evidence suggests that GSH decrement is required for efficient activation of an inflammatory condition and, at the same time, GSH-C4 can be envisaged as a good candidate to abrogate such process, expanding the anti-inflammatory role of this molecule in chronic inflammatory states.</p>