Effects and molecular mechanism of benserazide hydrochloride on LPS-induced inflammation in human umbilical vein endothelial cells
10.11665/j.issn.1000-5048.20180516
- VernacularTitle:盐酸苄丝肼对脂多糖所致人脐静脉内皮细胞炎症的影响及其机制研究
- Author:
Wei YANG
1
;
Shaoda WANG
;
Shujie QIN
;
Gang WU
;
Shuying HE
Author Information
1. 中国药科大学生命科学与技术学院
- Publication Type:Journal Article
- Keywords:
benserazide hydrochloride;
human umbilical vein endothelial cells;
inflammatory cytokines;
atherosclerosis;
lipopolysaccharides
- From:
Journal of China Pharmaceutical University
2018;49(5):624-631
- CountryChina
- Language:Chinese
-
Abstract:
In this article, human umbilical vein endothelial cells(HUVECs)were induced by lipopolysaccharides(LPS)to establish an in vitro inflammation model to further verify the anti-inflammation effects of benserazide hydrochloride and to explore the molecular mechanisms involving in the anti-inflammation and anti-atherosclerosis of benserazide hydrochloride. The experiments were divided into blank groups(PBS+0. 5% FBS DMEM medium), model group ［LPS(500 μg/mL)+ 0. 5% FBS DMEM medium］ and drug group ［LPS(500 μg/mL)+benserazide hydrochloride+0. 5% FBS DMEM medium］. Western blot, ELISA and qPCR were used to detect the protein and mRNA expression levels of inflammatory cytokines SAP, TNF-α and MCP-1 in HUVECs cells. The expression levels of p65/p-p65, p38/p-p38, IκBα/p-IκBα, AKT/p-AKT and the nuclear translocations of p65, p38 and IκBα were detected by Western blot. The results showed that benserazide hydrochloride(1×10-9, 1×10-10, 1×10-11 mol/L)could significantly inhibit the protein and mRNA expression of pro-inflammatory cytokines SAP, TNF-α and MCP-1. Besides, it could down-regulate the protein expression of p65/p-p65, p38/p-p38, IκBα/p-IκBα and AKT/p-AKT in the signal pathway while inhibiting the nuclear translocation of p65, p38 and IκBα, thereby inhibiting the transcriptional activity of the related genes.
