FGF19 alleviates inflammatory injury in vascular endothelial cells by activating the Nrf2/HO-1 signaling pathway.
10.7499/j.issn.1008-8830.2411076
- Author:
Yan-Jun ZHANG
1
;
Fei-Fei XIAO
1
;
Xiao-Hua LI
1
;
Shen-Hua TANG
1
;
Yi SANG
1
;
Chao-Yue LIU
1
;
Jian-Chang LI
1
Author Information
1. Department of Pediatrics, Affiliated Hospital of Binzhou Medical University, Binzhou, Shandong 256603, China.
- Publication Type:Journal Article
- Keywords:
Fibroblast growth factor19;
Human umbilical vein endothelial cell;
Inflammation;
Oxidative stress;
Type 1 diabetes mellitus;
Vascular endothelial dysfunction
- MeSH:
Humans;
NF-E2-Related Factor 2/genetics*;
Signal Transduction;
Human Umbilical Vein Endothelial Cells/drug effects*;
Fibroblast Growth Factors/pharmacology*;
Heme Oxygenase-1/physiology*;
Apoptosis/drug effects*;
Glucose;
Inflammation;
Interleukin-6/analysis*;
Vascular Endothelial Growth Factor A/genetics*;
Nitric Oxide Synthase Type II/analysis*;
Cells, Cultured
- From:
Chinese Journal of Contemporary Pediatrics
2025;27(5):601-608
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVES:To investigate the role and mechanism of fibroblast growth factor (FGF) 19 in inflammation-induced injury of vascular endothelial cells caused by high glucose (HG).
METHODS:Human umbilical vein endothelial cells (HUVECs) were randomly divided into four groups: control, HG, FGF19, and HG+FGF19 (n=3 each). The effect of different concentrations of glucose and/or FGF19 on HUVEC viability was assessed using the CCK8 assay. Flow cytometry was utilized to examine the impact of FGF19 on HUVEC apoptosis. Levels of interleukin-6 (IL-6), inducible nitric oxide synthase (iNOS), total superoxide dismutase (T-SOD), and malondialdehyde (MDA) were measured by ELISA. Real-time quantitative PCR and Western blotting were used to determine the mRNA and protein expression levels of vascular endothelial growth factor (VEGF), nuclear factor erythroid 2 related factor 2 (Nrf2), and heme oxygenase-1 (HO-1). Cells were further divided into control, siRNA-Nrf2 (siNrf2), HG, HG+FGF19, HG+FGF19+negative control, and HG+FGF19+siNrf2 groups (n=3 each) to observe the effect of FGF19 on oxidative stress injury in HUVECs induced by high glucose after silencing the Nrf2 gene.
RESULTS:Compared to the control group, the HG group exhibited increased apoptosis rate, increased IL-6, iNOS and MDA levels, and increased VEGF mRNA and protein expression, along with decreased T-SOD activity and decreased mRNA and protein expression of Nrf2 and HO-1 (P<0.05). Compared to the HG group, the HG+FGF19 group showed reduced apoptosis rate, decreased IL-6, iNOS and MDA levels, and decreased VEGF mRNA and protein expression, with increased T-SOD activity and increased Nrf2 and HO-1 mRNA and protein expression (P<0.05). Compared to the HG+FGF19+negative control group, the HG+FGF19+siNrf2 group had decreased T-SOD activity and increased MDA levels (P<0.05).
CONCLUSIONS:FGF19 can alleviate inflammation-induced injury in vascular endothelial cells caused by HG, potentially through the Nrf2/HO-1 signaling pathway.
