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Antioxidant activity of Hydroxytyrosol and Vitamin E reduces systemic inflammation in children with paediatric NAFLD.

Authors :
Mosca, Antonella
Crudele, Annalisa
Smeriglio, Antonella
Braghini, Maria Rita
Panera, Nadia
Comparcola, Donatella
Alterio, Arianna
Sartorelli, Maria Rita
Tozzi, Giulia
Raponi, Massimiliano
Trombetta, Domenico
Alisi, Anna
Source :
Digestive & Liver Disease; Sep2021, Vol. 53 Issue 9, p1154-1158, 5p
Publication Year :
2021

Abstract

The rise in paediatric non-alcoholic fatty liver disease (NAFLD) is particularly alarming. We recently reported that Hydroxytyrosol (HXT) and Vitamin E (VitE) may improve oxidative stress, insulin resistance, and steatosis in children with biopsy-proven NAFLD. Here, we investigated if HXT+VitE may reduce systemic inflammation in the above-mentioned patients. This study analysed the plasma levels of IL (interleukin)-6, IL-1β, IL-10, tumour necrosis factor (TNF)-α, 4‑hydroxy-2-nonenal (4-HNE) and 8-hydroxy-2′deoxyguanosine (8-OHdG) in children enrolled in the HXT+VitE trial (ClinicalTrials.gov, NCT02842567). Changes in markers of systemic inflammation were found in both placebo (Pla) and HXT+VitE. In particular, after four months, the levels of IL-1β and TNF-α were reduced in both groups, while IL-6 decreased, and IL-10 increased significantly only in the group treated with HXT+VitE. Children treated with HXT+VitE showed a significant decrease of 4-HNE and 8-OHdG that correlated with the improvement of triglyceride levels. Noticeably, only the 8-OHdG decrease correlated with steatosis amelioration and with the increase of IL-10 levels. The treatment with HXT and VitE reduced the NAFLD-related systemic inflammation in children, mainly by an increase of IL-10 circulating levels that occurred in response to DNA damage recovery, ultimately improving steatosis and hypertriglyceridemia. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
15908658
Volume :
53
Issue :
9
Database :
Supplemental Index
Journal :
Digestive & Liver Disease
Publication Type :
Academic Journal
Accession number :
151832132
Full Text :
https://doi.org/10.1016/j.dld.2020.09.021