Alcohol consumption is customary in many cultures and it is a common human behavior worldwide. Binge
ethanol and chronic alcohol consumption, two usual drinking patterns of human beings, produce a state of oxidative stress in liver and disturb the liver function. However, a safe and effective
therapy for
alcoholic liver disease in humans is still elusive. This study identified the
natural product berberine as a potential agent for treating or preventing
ethanol-induced liver injury. We demonstrated that
berberine attenuated oxidative stress resulted from
binge drinking in liver by reducing hepatic lipid peroxidation,
glutathione exhaust and mitochondrial oxidative damage. Furthermore,
berberine also prevented the oxidative stress and macrosteatosis in response to chronic
ethanol exposure in mice. Either the total
cytochrome P450 2E1 or the mitochondria-located
cytochrome P450 2E1, which is implicated in
ethanol-mediated oxidative stress, was suppressed by
berberine. On the other hand,
berberine significantly blunted the
lipid accumulation in liver due to chronic alcohol consumption, at least partially, through restoring
peroxisome proliferator-activated receptor α/
peroxisome proliferator-activated receptor-gamma Co-activator-1α and
hepatocyte nuclear factor 4α/
microsomal triglyceride transfer protein pathways. These findings suggested that
berberine could serve as a potential agent for preventing or treating human
alcoholic liver disease.