Guanxin Zhitong Capsules attenuate human endothelial cell damage induced by palmitic acid via MAPK signaling pathway.
10.19540/j.cnki.cjcmm.20210726.701
- Author:
Xiao-Li WANG
1
;
Jing SHAO
2
;
Guan-Xin WU
2
;
Wei ZHANG
1
;
Hong-Yan ZHOU
1
;
Kai-Yan LI
1
;
Wei SUN
1
Author Information
1. Henan Academy of Chinese Medicine Zhengzhou 450004, China.
2. the First Affiliated Hospital of Henan University of Chinese Medicine Zhengzhou 450000, China.
- Publication Type:Journal Article
- Keywords:
Guanxin Zhitong Capsules;
MAPK signaling pathway;
atherosclerosis;
human umbilical vein endothelial cells;
palmitic acid
- MeSH:
Apoptosis;
Capsules;
Human Umbilical Vein Endothelial Cells/metabolism*;
Humans;
MAP Kinase Signaling System;
Palmitic Acid/toxicity*;
Signal Transduction;
p38 Mitogen-Activated Protein Kinases/metabolism*
- From:
China Journal of Chinese Materia Medica
2021;46(19):5096-5102
- CountryChina
- Language:Chinese
-
Abstract:
The present study observed the effect of Guanxin Zhitong Capsules(GXZT) on the lipotoxicity of vascular endothelial cells and investigated the mechanism of GXZT in atherosclerosis treatment. The lipotoxicity model in human umbilical vein endothelial cells(HUVECs) was induced by palmitic acid(PA) stimulation. These cells were divided into a normal control group(NC, 15% normal serum), a model group(PA, 0.6 mmol·L~(-1) PA+15% normal serum), a high-dose GXZT group(GXZT-H, 0.6 mmol·L~(-1) PA+15% GXZT-medicated serum), a medium-dose GXZT group(GXZT-M, 0.6 mmol·L~(-1) PA+10% GXZT-medicated serum+5% normal serum) and a low-dose GXZT group(GXZT-L, 0.6 mmol·L~(-1) PA+5% GXZT-medicated serum+10% normal serum). HUVECs were detected for cell viability by cell counting kit-8(CCK-8) assay, apoptosis by flow cytometry, mitochondrial membrane potential(MMP) by JC-1 labeled laser scanning confocal microscopy, and total and phosphorylated proteins of p38, ERK1/2, and JNK1/2 in the mitogen-activated protein kinases(MAPK) signaling pathway by Western blot. The phosphorylated level was calcula-ted. Compared with the NC group, the PA group showed decreased cell viability and MMP(P<0.01, P<0.01), elevated apoptosis(P<0.01), and up-regulated phosphorylated levels of p38, ERK1/2, and JNK1/2(P<0.01, P<0.01, P<0.01). Compared with the PA group, the GXZT-H, GXZT-M, and GXZT-L groups showed increased cell viability and MMP(P<0.01, P<0.01, P<0.01), reduced apoptosis(P<0.01), and down-regulated protein expression and phosphorylated levels of p38, ERK1/2 and JNK1/2 in the MAPK signaling pathway(P<0.01, P<0.01, P<0.01). In conclusion, the results suggest that GXZT functions via blocking MAPK signaling pathway to relieve the damage of HUVECs induced by PA.
