Aloe-emodin quinone pretreatment reduces acute liver injury induced by carbon tetrachloride.

Aloe contains several active compounds including aloin, a C-glycoside that can be hydrolyzed in the gut to form aloe-emodin anthrone which, in turn, is auto-oxidized to the quinone aloe-emodin. On the basis of the claimed hepatoprotective activity of some antraquinones, we studied aloe-emodin in a rat model of carbon tetrachloride (CCl 4 ) intoxication, since this xenobiotic induces acute liver damage by lipid peroxidation subsequent to free radical production. Twelve rats were treated with CCl 4 (3 mg/kg) intraperitoneally and six were protected with two intraperitoneally injections of aloe-emodin (50 mg/kg: CCl 4 +aloe-emodin); six other rats were only aloe-emodin injected (aloe-emodin) and six were untreated (control). Histological examination of the livers showed less marked lesions in the CCl 4 +aloe-emodin rats than in those treated with CCl 4 alone, and this was confirmed by the serum levels of L-aspartate-2-oxoglutate-aminotransferase (394±38.6 UI/l in CCl 4 , 280±24.47 UI/l in CCl 4 +aloe-emodin rats; P<0.05). We also quantified changes in hepatic albumin and tumour necrosis factor-a mRNAs. Albumin mRNA expression was significantly lower only in the liver of CCl 4 rats (P<0.05 versus control) and was only slightly reduced in the CCl 4 +aloe-emodin rats. In contrast tumour necrosis factor-a mRNA was significantly higher (P<0.05) in the CCl 4 than the control rats and almost equal in the CCl 4 +aloe-emodin, aloe-emodin and control groups. In conclusion, aloe-emodin appears to have some protective effect not only against hepatocyte death but also on the inflammatory response subsequent to lipid peroxidation.