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. 2014 Sep;86(3):284–296. doi: 10.1124/mol.114.093039

Fig. 7.

Fig. 7.

Proposed model for the modulation of ethanol-induced Nox2 expression by globular adiponectin and its potential role in the suppression of ethanol-induced ROS production in macrophages. Ethanol treatment induces increase in ROS production in murine macrophages via NADPH oxidase activation, which is composed of various cytosolic and membrane subunits. Ethanol-induced NADPH oxidase activation is accompanied with Nox2 expression through the p38 MAPK/NF-κB pathway. Globular adiponectin treatment results in prevention of ROS production induced by ethanol treatment. The inhibitory effect of gAcrp on ethanol-induced ROS production is mediated by modulation of NADPH oxidase, particularly via inhibition of Nox2 expression. Abrogation of ethanol-induced Nox2 expression by globular adiponectin is mediated through LKB1/AMPK axis signaling mechanisms. LKB1 and AMPK signaling pathway reverted ethanol-induced Nox2 expression, probably via negative regulation of transcriptional activity of NF-κB. Detailed mechanisms underlying inhibition of NF-κB signaling by LKB1/AMPK axis remain to be determined.