Sodium butyrate potentiates carbon tetrachloride-induced acute liver injury in mice.

Histone deacetylase 2 (HDAC2), a prominent member of the class I HDAC family, plays crucial roles in inflammation and other pathological processes. Recent studies have found that the activity and expression of HDAC2 were altered under oxidative stress conditions. The aim of the current study was to elucidate the expression and the possible pathophysiological significance of HDAC2 in CCl(4)-induced oxidative hepatitis. Our resultant data indicated that the expression of HDAC2 in liver increased after CCl(4) exposure, which was attenuated by antioxidants N-acetyl-L-cysteine or α-lipoic acid. Administration of sodium butyrate (NaB), a representative HDAC inhibitor resulted in further elevation of serum aminotransferase levels, enhanced oxidative stress, reduced antioxidant enzyme activities, increased production of proinflammatory cytokines and aggravated hepatocellular necrosis as well as leukocyte infiltration in liver. The results suggested that oxidative stress in CCl(4)-exposed mice induce the expression of HDAC2, while inhibition of HDAC result in exacerbated liver injury. Therefore, HDAC might be involved in the pathogenesis of CCl(4)-induced liver injury and provide protective benefit.