Aloe‐Emodin Quinone Pretreatment Reduces Acute Liver Injury Induced by Carbon Tetrachloride

Abstract

Abstract: 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‐α 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‐α 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.