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

Authors: Arosio B.1; Gagliano N.1; Fusaro L.M.P.1; Parmeggiani L.1; Tagliabue J.1; Galetti P.1; de Castri D.2; Moscheni C.1; Annoni G.3

Source: Basic & Clinical Pharmacology & Toxicology, Volume 87, Number 5, 1 November 2000 , pp. 229-233(5)

Publisher: Blackwell Publishing

Key:
Free Content - Free Content
New Content - New Content
Subscribed Content - Subscribed Content
Free Trial Content - Free Trial Content

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-agr 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-agr 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.

Document Type: Original article

Affiliations: 1: Department of Internal Medicine, Milano University Study and Hospital Maggiore IRCCS, Milano, 2: Center Maria Branca, Milano, Italy 3: School of Medicine, Milano-Bicocca University Study, and

* This feature is in beta and some links may initially be displayed as numbers instead of article titles. Clicking on any of the links will take you to the recommended articles, regardless of the display of the link.

The full text article is temporarily unavailable.

We apologise for the inconvenience. Please try again later.

Back to top

Key:
Free Content - Free Content
New Content - New Content
Subscribed Content - Subscribed Content
Free Trial Content - Free Trial Content
Page Help Click here for Page Help
Shopping cart
Tools
Sign in






Need to register?
Sign up here
Text size: A | A | A | A