Resveratrol increases sirtuin 1 expression in peripheral blood mononuclear cells of premature infants and inhibits the oxidative stress induced by hyperoxia in vivo.
- Author:
Xi YANG
1
;
Wen-Bin DONG
;
Qing-Ping LI
;
Lan KANG
;
Xiao-Ping LEI
;
Lian-Yu ZHANG
;
You-Ying LU
;
Xue-Song ZHAI
Author Information
- Publication Type:Journal Article
- MeSH: Female; Humans; Hyperoxia; metabolism; Infant, Newborn; Infant, Premature; Leukocytes, Mononuclear; metabolism; Lipid Peroxidation; Male; Oxidative Stress; Sirtuin 1; blood; Stilbenes; pharmacology
- From: Chinese Journal of Contemporary Pediatrics 2016;18(1):72-77
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the effect of resveratrol on the levels of sirtuin 1 (SIRT1) and reactive oxygen species (ROS) in peripheral blood mononuclear cells (PBMCs) of premature infants exposed to hyperoxia.
METHODSPeripheral blood and isolated PBMCs from premature infants (gestational age<32 weeks) without oxygen supplement were collected and were randomly assigned into four groups: control, air+resveratrol, hyperoxia, and hyperoxia+resveratrol. The PBMCs were cultured in vitro for 48 hours, then the ROS content in PBMCs was measured by laser scanning confocal microscopy. Malondialdehyde (MDA) content in the medium was measured by the whole spectrum spectrophotometer. SIRT1 positioning was assessed by immunofluorescence. SIRT1 expression levels in PBMCs were measured by Western bolt.
RESULTSCompared with the control group, the level of SIRT1 in the air+resveratrol group increased significantly (P<0.05). The levels of ROS and MDA and the SIRT1 transposition rate in the hyperoxia group increased significantly, while the expression level of SIRT1 decreased significantly compared with the control group (P<0.05). The levels of ROS and MDA and the SIRT1 transposition rate decreased significantly (P<0.05), and the expression level of SIRT1 increased significantly in the hyperoxia+resveratrol group (P<0.05).
CONCLUSIONSResveratrol can increase SIRT1 expression in PBMCs and inhibit SIRT1 shuttle from nucleus to cytoplasm in order to increase the ability of antioxidative stress in premature infants exposed to hyperoxia, thereby reducing the oxidative stress injury in premature infants.