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Effects of naringin and valproate interaction on liver steatosis and dyslipidaemia parameters in male C57BL6 mice

Authors
  • Jutrić, David1, 2
  • Đikić, Domagoj1
  • Boroš, Almoš1
  • Odeh, Dyna1
  • Drozdek, Sandra Domjanić3
  • Gračan, Romana1
  • Dragičević, Petar4
  • Crnić, Irena5
  • Jurčević, Irena Landeka5
  • 1 University of Zagreb Faculty of Science, Croatia , (Croatia)
  • 2 Clinical Hospital Dubrava, Croatia , (Croatia)
  • 3 University of Applied Health Sciences, Croatia , (Croatia)
  • 4 University of Zagreb School of Medicine, Croatia , (Croatia)
  • 5 University of Zagreb Faculty of Food Technology and Biotechnology, Croatia , (Croatia)
Type
Published Article
Journal
Archives of Industrial Hygiene and Toxicology
Publisher
Sciendo
Publication Date
Apr 07, 2022
Volume
73
Issue
1
Pages
71–82
Identifiers
DOI: 10.2478/aiht-2022-73-3608
Source
De Gruyter
Keywords
Disciplines
  • Original article
License
Green

Abstract

Valproate is a common antiepileptic drug whose adverse effects include liver steatosis and dyslipidaemia. The aim of our study was to see how natural flavonoid antioxidant naringin would interact with valproate and attenuate these adverse effects. For this reason we treated male C57BL6 mice with a combination of 150 mg/kg of valproate and 25 mg/kg naringin every day for 10 days and compared their serum triglycerides, cholesterol, LDL, HDL, VLDL, and liver PPAR-alpha, PGC-1 alpha, ACOX1, Nrf2, SOD, CAT, GSH, and histological signs of steatosis. Valproate increased lipid peroxidation parameters and caused pronounced microvesicular steatosis throughout the hepatic lobule in all acinar zones, but naringin co-administration limited steatosis to the lobule periphery. In addition, it nearly restored total serum cholesterol, LDL, and triglycerides and liver ACOX1 and MDA to control levels. and upregulated PPAR-alpha and PGC-1 alpha, otherwise severely downregulated by valproate. It also increased SOD activity. All these findings suggest that naringin modulates key lipid metabolism regulators and should further be investigated in this model, either alone or combined with other lipid regulating drugs or molecules.

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