Albiflorin Alleviates Ox-LDL-Induced Human Umbilical Vein Endothelial Cell Injury through IRAK1/TAK1 Pathway

Autor:	Yeling Liu, Yilai Sun, Xue Bai, Lingxing Li, Guihua Zhu
Rok vydání:	2022
Předmět:	Bridged-Ring Compounds Inflammation Article Subject General Immunology and Microbiology Apoptosis General Medicine Atherosclerosis General Biochemistry Genetics and Molecular Biology Lipoproteins LDL Cholesterol Interleukin-1 Receptor-Associated Kinases Human Umbilical Vein Endothelial Cells Humans Reactive Oxygen Species
Zdroj:	BioMed research international. 2022
ISSN:	2314-6141
Popis:	Introduction. Atherosclerosis (AS) is a chronic inflammatory disease characterized by lipid metabolism disorder and vascular endothelial damage. Albiflorin (AF) has been certified to be effective in the therapy of certain inflammatory diseases, while the therapeutic effect and mechanism of AF on AS have not been fully elucidated. Material and Methods. Model cells for AS were created by inducing oxidized low-density lipoprotein (Ox-LDL) in human umbilical vein endothelial cells (HUVECs). After processing with AF and interleukin-1 receptor-associated kinase 1- (IRAK1-) overexpressed plasmid, cell viability was assessed by CCK-8; cholesterol efflux was tested using liquid scintillation counter; IL-6 and TNF-α levels were determined with ELISA kits; ROS and apoptosis were confirmed using Flow cytometry. Besides, IRAK1-TAK1 pathway and apoptosis- and mitochondrial fusion-related proteins were monitored with western blotting analysis. Results. Our results verified that AF could not only dramatically accelerate viability and cholesterol efflux but also attenuate inflammation, ROS production, and apoptosis in Ox-LDL-induced HUVECs. Meanwhile, AF could prominently prevent the activation of IRAK1-TAK1 pathway, downregulate apoptosis-related proteins, and upregulate mitochondrial fusion-related proteins in Ox-LDL-induced HUVECs. Moreover, we testified that IRAK1 overexpression memorably could reverse suppression of AF on inflammation, apoptosis, and IRAK1-TAK1 pathway and enhancement of AF on viability, cholesterol efflux, and mitochondrial fusion in Ox-LDL-induced HUVECs. Conclusions. By blocking the IRAK1/TAK1 pathway, AF can significantly slow the course of AS, suggesting that it could be a viable therapeutic option for AS.
Databáze:	OpenAIRE
Externí odkaz:	https://explore.openaire.eu/search/publication?articleId=doi_dedup___::2c2d6f4cf8913edb53058fb22f0baf3c https://pubmed.ncbi.nlm.nih.gov/35601145 Zobrazit plný text záznamu Plný text ve formátu PDF Plný text ve formátu HTML
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