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Nutrients 2017, 9(10), 1086; doi:10.3390/nu9101086

Silibinin Restores NAD+ Levels and Induces the SIRT1/AMPK Pathway in Non-Alcoholic Fatty Liver

1
Division of Gastroenterology, Acireale Hospital, Azienda Sanitaria Provinciale di Catania, 95124 Catania, Italy
2
Department of Drug Sciences, University of Catania, 95125 Catania, Italy
3
Department of Biomedical and Biotechnological Sciences, University of Catania, 95123 Catania, Italy
4
Department of Clinical Medicine and Surgery, University of Naples “Federico II”, 80131 Naples, Italy
5
Division of Laboratory Medicine, Hospital “Garibaldi”, 95124 Catania, Italy
6
Department of Medical, Oral and Biotechnological Sciences, University of Chieti, 66013 Chieti, Italy
*
Author to whom correspondence should be addressed.
Received: 18 July 2017 / Revised: 14 September 2017 / Accepted: 19 September 2017 / Published: 30 September 2017
(This article belongs to the Special Issue Effects of Polyphenol-Rich Foods on Human Health)
View Full-Text   |   Download PDF [1427 KB, uploaded 30 September 2017]   |  

Abstract

Nicotinamide adenine dinucleotide (NAD+) homeostasis is emerging as a key player in the pathogenesis of non-alcoholic fatty liver disease (NAFLD) and is tightly linked to the SIRT1/5’-AMP-activated protein kinase (AMPK) pathway. Silibinin, the main component of silymarin, has been proposed as a nutraceutical for the treatment of NAFLD. In this study, we aimed to identify whether silibinin may influence the NAD+/SIRT1 axis. To this end, C57BL/6 mice were fed a high fat diet (HFD) for 16 weeks, and were treated with silibinin or vehicle during the last 8 weeks. HepG2 cells were treated with 0.25 mM palmitate for 24 h with silibinin 25 µM or vehicle. HFD and palmitate administration led to oxidative stress, poly-(ADP-ribose)-polymerase (PARP) activation, NAD+ consumption, and lower SIRT1 activity. In mice fed the HFD, and in HepG2 treated with palmitate, we consistently observed lower levels of phospho-AMPKThr172 and phospho-acetyl-CoA carboxylaseSer79 and higher levels of nuclear sterol regulatory element-binding protein 1 activity, indicating de novo lipogenesis. Treatment of mice and HepG2 with silibinin abolished oxidative stress, and inhibited PARP activation thus restoring the NAD+ pool. In agreement with preserved NAD+ levels, SIRT1 activity and AMPK phosphorylation returned to control levels in mice and HepG2. Our results further indicate silibinin as a promising molecule for the treatment of NAFLD. View Full-Text
Keywords: silibinin; NAD+; SIRT1; AMPK; lipogenesis silibinin; NAD+; SIRT1; AMPK; lipogenesis
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Salomone, F.; Barbagallo, I.; Godos, J.; Lembo, V.; Currenti, W.; Cinà, D.; Avola, R.; D’Orazio, N.; Morisco, F.; Galvano, F.; Li Volti, G. Silibinin Restores NAD+ Levels and Induces the SIRT1/AMPK Pathway in Non-Alcoholic Fatty Liver. Nutrients 2017, 9, 1086.

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