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Open AccessArticle

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

1
Liver Unit of “Bambino Gesù” Children’s Hospital, IRCCS, Rome 00165, Italy
2
Laboratory of Biochemistry, of “Bambino Gesù” Children’s Hospital, IRCCS, Rome 00165, Italy
3
Department of Biology and Biotechnology “C. Darwin”, “La Sapienza” University, Rome 00185, Italy
4
Department of Basic and Applied Biology, University of L’Aquila, L’Aquila 67010, Italy
5
Neuromuscular and Neurodegenerative Disease Unit, “Bambino Gesù” Children’s Hospital, IRCCS, Rome 00165, Italy
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2012, 13(2), 2276-2289; https://doi.org/10.3390/ijms13022276
Received: 9 January 2012 / Revised: 7 February 2012 / Accepted: 9 February 2012 / Published: 20 February 2012
(This article belongs to the Special Issue Antioxidants)
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. View Full-Text
Keywords: hepatosteatosis; emodin; high fat diet; high fructose diet; redox status hepatosteatosis; emodin; high fat diet; high fructose diet; redox status
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.

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