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, i s auto-oxidized to the quinone aloe-emodin. On the basis of the claimed hep atoprotective activity of some antraquinones, we studied aloe-emodin in a r at model of carbon tetrachloride (CCl4) intoxication, since this xenobiotic induces acute liver damage by lipid peroxidation subsequent to free radica l production. Twelve rats were treated with CCl4 (3 mg/kg) intraperitoneall y and six were protected with two intraperitoneally injections of aloe-emod in (50 mg/kg; CCl4+aloe-emodin); six other rats were only aloe-emodin injec ted (aloe-emodin) and six were untreated (control). Histological examinatio n of the livers showed less marked lesions in the CCl4+aloe-emodin rats tha n in tho se treated wi th CCl4 alone, and this was confirmed by the serum l evels of L-aspartate-2- oxoglutate-aminotransferase (394+/-38.6 UI/l in CCl 4, 280+/-24.47 UI/l in CCl4+aloe-emodin rats; P<0.05). We also quantified c hanges in hepatic albumin and tumour necrosis factor-<alpha> mRNAs. Albumin mRNA expression was significantly lower only in the liver of CCl4 rats (P< 0.05 versus control) and was only slightly reduced in the CCl4+aloe-emodin rats. In contrast tumour necrosis factor-<alpha> mRNA was significantly hig her (P<0.05) in the CCl4, than the control rats and almost equal in the CCl 4+aloe-emodin, aloe-emodin and control groups. In conclusion, aloe-emodin a ppears to have some protective effect not only against hepatocyte death but also on the inflammatory response subsequent to lipid peroxidation.