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; P4 rats (P4+aloe-emodin rats. In contrast tumour necrosis factor-α mRNA was significantly higher (P4 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.
| Original language | English |
|---|---|
| Pages (from-to) | 229-233 |
| Number of pages | 5 |
| Journal | Pharmacology and Toxicology |
| Volume | 87 |
| Issue number | 5 |
| Publication status | Published - Nov 2000 |
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ASJC Scopus subject areas
- Health, Toxicology and Mutagenesis
- Pharmacology
- Toxicology
Cite this
Aloe-emodin quinone pretreatment reduces acute liver injury induced by carbon tetrachloride. / Arosio, B.; Gagliano, N.; Fusaro, L. M P; Parmeggiani, L.; Tagliabue, J.; Galetti, P.; De Castri, D.; Moscheni, C.; Annoni, G.
In: Pharmacology and Toxicology, Vol. 87, No. 5, 11.2000, p. 229-233.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Aloe-emodin quinone pretreatment reduces acute liver injury induced by carbon tetrachloride
AU - Arosio, B.
AU - Gagliano, N.
AU - Fusaro, L. M P
AU - Parmeggiani, L.
AU - Tagliabue, J.
AU - Galetti, P.
AU - De Castri, D.
AU - Moscheni, C.
AU - Annoni, G.
PY - 2000/11
Y1 - 2000/11
N2 - 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; P4 rats (P4+aloe-emodin rats. In contrast tumour necrosis factor-α mRNA was significantly higher (P4 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.
AB - 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; P4 rats (P4+aloe-emodin rats. In contrast tumour necrosis factor-α mRNA was significantly higher (P4 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.
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M3 - Article
C2 - 11129503
AN - SCOPUS:0033678216
VL - 87
SP - 229
EP - 233
JO - Pharmacology and Toxicology
JF - Pharmacology and Toxicology
SN - 0901-9928
IS - 5
ER -