Active form of vitamin D ameliorates non-alcoholic fatty liver disease by alleviating oxidative stress in a high-fat diet rat model.

Autor: Zhu CG; Department of Endocrinology, Tianjin Medical University General Hospital, Tianjin 300052, China., Liu YX; Department of Endocrinology, Tianjin Medical University General Hospital, Tianjin 300052, China., Wang H; Department of Endocrinology, Tianjin Medical University General Hospital, Tianjin 300052, China., Wang BP; Department of Endocrinology, Tianjin Medical University General Hospital, Tianjin 300052, China., Qu HQ; Department of Paediatrics, Division of Endocrinology, McGill University Health Centre Research Institute, Montréal H4A 3J1, Canada., Wang BL; Key Lab of Hormones and Development (Ministry of Health), Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin 300052, China., Zhu M; Department of Endocrinology, Tianjin Medical University General Hospital, Tianjin 300052, China.
Jazyk: angličtina
Zdroj: Endocrine journal [Endocr J] 2017 Jul 28; Vol. 64 (7), pp. 663-673. Date of Electronic Publication: 2017 May 23.
DOI: 10.1507/endocrj.EJ16-0542
Abstrakt: The purpose of this study was to determine whether treatment using the active form of vitamin D (1,25(OH) 2 D 3 ) could protect against high-fat diet (HFD)-induced non-alcoholic fatty liver disease (NAFLD) in rats and ameliorate oxidative stress. Male Sprague-Dawley rats were divided into three groups and treated with standard chow, HFD, or HFD plus intraperitoneal injection of 1,25(OH) 2 D 3 (5 μg/kg body weight, twice per week), respectively, for 16 weeks. Serum lipid profiles, hepatic function, intrahepatic lipid, and calcium levels were determined. Hepatic histology was examined using hematoxylin/eosin, Masson's trichrome, and Oil Red O staining. Oxidative stress was assessed by measuring hepatic malondialdehyde (MDA) and F2α-isoprostane content. Expression of nuclear factor-erythroid-2-related factor 2 (Nrf2) and downstream target genes was analyzed using quantitative RT-PCR. 1,25(OH) 2 D 3 treatment improved the serum lipid profile, reduced intrahepatic lipid levels, and attenuated hepatic steatosis and inflammation in HFD rats. Furthermore, MDA and F2α-isoprostane levels in liver tissue were reduced by 1,25(OH) 2 D 3 administration. Although 1,25(OH) 2 D 3 did not regulate the expression of Nrf2 mRNA, it did induce Nrf2 nuclear translocation. The expression of Nrf2 target genes, including Gclc, Nqo1, Sod2, and Cat, was up-regulated by 1,25(OH) 2 D 3 . We conclude that 1,25(OH) 2 D 3 protects against HFD-induced NAFLD by attenuating oxidative stress, inducing NRF2 nuclear translocation, and up-regulating the expression of genes encoding antioxidant enzymes.
Databáze: MEDLINE