title: Aloe-Emodin quinone pretreatment reduces acute liver injury induced by carbon tetrachloride.
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 (CCl4) intoxication, since this xenobiotic induces acute liver damage by lipid peroxidation subsequent to free radical production. Twelve rats were treated with CCl4 (3 mg/kg) intraperitoneally and six were protected with two intraperitoneally injections of aloe-emodin (50 mg/kg; CCl4+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 CCl4+aloe-emodin rats than in those treated with CCl4 alone, and this was confirmed by the serum levels of L-aspartate-2-oxoglutate-aminotransferase (394+/-38.6 UI/l in CCl4, 280+/-24.47 UI/l in CCl4+aloe-emodin rats; P<0.05). We also quantified changes 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 higher (P<0.05) in the CCl4 than the control rats and almost equal in the CCl4+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.
authors: Department of Internal Medicine, Milano University Study and Hospital Maggiore IRCCS, Italy.
authors: B
authors: B
authors: Arosio
authors: N
authors: N
authors: Gagliano
authors: L M
authors: LM
authors: Fusaro
authors: L
authors: L
authors: Parmeggiani
authors: J
authors: J
authors: Tagliabue
authors: P
authors: P
authors: Galetti
authors: D
authors: D
authors: De Castri
authors: C
authors: C
authors: Moscheni
authors: G
authors: G
authors: Annoni
mesh_terms: D000418:Albumins / Q000235:genetics / Q000378:metabolism; D000818:Animals; D000880:Anthraquinones; D000970:Antineoplastic Agents / Q000627:therapeutic use*; D001219:Aspartate Aminotransferases / Q000097:blood; D015152:Blotting, Northern; D002251:Carbon Tetrachloride / Q000633:toxicity*; D056486:Chemical and Drug Induced Liver Injury / Q000097:blood / Q000209:etiology / Q000517:prevention & control*; D004195:Disease Models, Animal; D004347:Drug Interactions; D004642:Emodin / Q000031:analogs & derivatives* / Q000627:therapeutic use*; D007274:Injections, Intraperitoneal; D008099:Liver / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008297:Male; D012333:RNA, Messenger / Q000302:isolation & purification / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: D000418:Albumins; D000880:Anthraquinones; D000970:Antineoplastic Agents; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; C059635:aloe emodin anthrone; C518327:aloe emodin; D002251:Carbon Tetrachloride; D001219:Aspartate Aminotransferases; D004642:Emodin