Int. J. Mol. Sci. 2012, 13(2), 2276-2289; doi:10.3390/ijms13022276
Article

Emodin Prevents Intrahepatic Fat Accumulation, Inflammation and Redox Status Imbalance During Diet-Induced Hepatosteatosis in Rats

1,* email, 2email, 1email, 1email, 1email, 3email, 4email, 5email, 5email and 1email
Received: 9 January 2012; in revised form: 7 February 2012 / Accepted: 9 February 2012 / Published: 20 February 2012
(This article belongs to the Special Issue Antioxidants)
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract: High-fat and/or high-carbohydrate diets may predispose to several metabolic disturbances including liver fatty infiltration (hepatosteatosis) or be associated with necro-inflammation and fibrosis (steatohepatitis). Several studies have emphasized the hepatoprotective effect of some natural agents. In this study, we investigated the potential therapeutic effects of the treatment with emodin, an anthraquinone derivative with anti-oxidant and anti-cancer abilities, in rats developing diet-induced hepatosteatosis and steatohepatitis. Sprague-Dawley rats were fed a standard diet (SD) for 15 weeks, or a high-fat/high-fructose diet (HFD/HF). After 5 weeks, emodin was added to the drinking water of some of the SD and HFD/HF rats. The experiment ended after an additional 10 weeks. Emodin-treated HFD/HF rats were protected from hepatosteatosis and metabolic derangements usually observed in HFD/HF animals. Furthermore, emodin exerted anti-inflammatory activity by inhibiting the HFD/HF-induced increase of tumor necrosis factor (TNF)-α. Emodin also affected the hepatocytes glutathione homeostasis and levels of the HFD/HF-induced increase of glutathionylated/phosphorylated phosphatase and tensin homolog (PTEN). In conclusion, we demonstrated that a natural agent such as emodin can prevent hepatosteatosis, preserving liver from pro-inflammatory and pro-oxidant damage caused by HFD/HF diet. These findings are promising, proposing emodin as a possible hindrance to progression of hepatosteatosis into steatohepatitis.
Keywords: hepatosteatosis; emodin; high fat diet; high fructose diet; redox status
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MDPI and ACS Style

Alisi, A.; Pastore, A.; Ceccarelli, S.; Panera, N.; Gnani, D.; Bruscalupi, G.; Massimi, M.; Tozzi, G.; Piemonte, F.; Nobili, V. Emodin Prevents Intrahepatic Fat Accumulation, Inflammation and Redox Status Imbalance During Diet-Induced Hepatosteatosis in Rats. Int. J. Mol. Sci. 2012, 13, 2276-2289.

AMA Style

Alisi A, Pastore A, Ceccarelli S, Panera N, Gnani D, Bruscalupi G, Massimi M, Tozzi G, Piemonte F, Nobili V. Emodin Prevents Intrahepatic Fat Accumulation, Inflammation and Redox Status Imbalance During Diet-Induced Hepatosteatosis in Rats. International Journal of Molecular Sciences. 2012; 13(2):2276-2289.

Chicago/Turabian Style

Alisi, Anna; Pastore, Anna; Ceccarelli, Sara; Panera, Nadia; Gnani, Daniela; Bruscalupi, Giovannella; Massimi, Mara; Tozzi, Giulia; Piemonte, Fiorella; Nobili, Valerio. 2012. "Emodin Prevents Intrahepatic Fat Accumulation, Inflammation and Redox Status Imbalance During Diet-Induced Hepatosteatosis in Rats." Int. J. Mol. Sci. 13, no. 2: 2276-2289.

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