Aloe-Emodin Quinone Pretreatment Reduces Acute Liver Injury Induced by Carbon Tetrachloride
Articolo
Data di Pubblicazione:
2000
Citazione:
Aloe-Emodin Quinone Pretreatment Reduces Acute Liver Injury Induced by Carbon Tetrachloride / B. Arosio, N. Gagliano, L.M.P. Fusaro, L. Parmeggiani, J. Tagliabue, P. Galetti, D. De Castri, C. Moscheni, G. Annoni. - In: PHARMACOLOGY & TOXICOLOGY. - ISSN 0901-9928. - 87:5(2000), pp. 229-233. [10.1034/j.1600-0773.2000.pto870507.x]
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; CCl4¹aloe-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 CCl4¹aloe-emodin rats than
in those treated with CCl4 alone, and this was confirmed by the serum levels of L-aspartate-2-oxoglutate-aminotransferase
(394º38.6 UI/l in CCl4, 280º24.47 UI/l in CCl4¹aloe-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
CCl4 rats (P,0.05 versus control) and was only slightly reduced in the CCl4¹aloe-emodin rats. In contrast tumour
necrosis factor-a mRNA was significantly higher (P,0.05) in the CCl4 than the control rats and almost equal in the
CCl4¹aloe-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.
Tipologia IRIS:
01 - Articolo su periodico
Elenco autori:
B. Arosio, N. Gagliano, L.M.P. Fusaro, L. Parmeggiani, J. Tagliabue, P. Galetti, D. De Castri, C. Moscheni, G. Annoni
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