Inhibition of heat shock protein 90 alleviates steatosis and macrophage activation in murine alcoholic liver injury.

ABSTRACT:

Background & aims

Heat shock protein 90 (hsp90) is an emerging therapeutic target in chronic liver diseases. Hsp90 plays an important role in liver immune cell activation; however its role in alcoholic liver disease (ALD) remains elusive. Here we hypothesize that hsp90 is crucial in alcohol induced steatosis and pro-inflammatory cytokine production. To test this hypothesis, we employed a pharmacological inhibitor of hsp90, 17-DMAG (17-Dimethylamino-ethylamino-17-demethoxygeldanamycin) in an in vivo mouse model of acute and chronic alcoholic liver injury.

Methods

C57BL/6 mice were given either a single dose of ethanol via oral gavage (acute) or chronically fed alcohol for 2 weeks followed by oral gavage (chronic-binge). 17-DMAG was administered during or at the end of feeding

SUBMITTER: Ambade A 

PROVIDER: S-EPMC4169725 | biostudies-literature | 2014 Oct

REPOSITORIES: biostudies-literature