Dataset Information

Atheroprotective Mechanisms of Tilianin by Inhibiting Inflammation Through Down-Regulating NF-?B Pathway and Foam Cells Formation.

ABSTRACT: Tilianin, a representative flavonoid ingredient of Dracocephalum moldavica L., has been used to treat several diseases for centuries, including atherosclerosis (AS). However, pharmacological mechanisms underlying its biological functions remain elusive. In the present study, we investigated the anti-AS mechanisms of tilianin through establishing in vitro models using three types of cells that contributed to AS progression, including macrophage, vascular smooth muscle cells and human umbilical vein endothelial cells, which were proved to be involve in LPS/TNF-?/oxidized low density lipoprotein (ox-LDL)-induced inflammation and ox-LDL induced foam cell formation. Our results indicate that tilianin significantly suppressed LPS induced inflammatory responses on macrophage and remarkably inhibited TNF-? induced VSMCs proliferation and migration. Furthermore, the anti-inflammatory effect of tilianin on macrophages and VSMCs was proved to be mainly by downregulating TNF-?/NF-?B pathway. Moreover, our results demonstrate that tilianin significantly ameliorated ox-LDL induced macrophages oriented foam cells formation through repressing mRNA expression of SR-A1 and inducting the expression of genes related to cholesterol efflux including SRB-1 and ABCA1. However, tilianin had no effect on ox-LDL induced HUVECs injury.

SUBMITTER: Shen W

PROVIDER: S-EPMC6614704 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Atheroprotective Mechanisms of Tilianin by Inhibiting Inflammation Through Down-Regulating NF-κB Pathway and Foam Cells Formation.

Shen Wanli W Anwaier Gulinigaer G Anwaier Gulinigaer G Cao Yini Y Lian Guan G Chen Cong C Liu Shu S Tuerdi Nuerbiye N Qi Rong R

Frontiers in physiology 20190702

Tilianin, a representative flavonoid ingredient of <i>Dracocephalum moldavica</i> L., has been used to treat several diseases for centuries, including atherosclerosis (AS). However, pharmacological mechanisms underlying its biological functions remain elusive. In the present study, we investigated the anti-AS mechanisms of tilianin through establishing <i>in vitro</i> models using three types of cells that contributed to AS progression, including macrophage, vascular smooth muscle cells and huma ...[more]

PMID: 31333487

Similar Datasets

Project description:BackgroundAdiponectin is an adipocytokine that plays a key regulatory role in glucose and lipid metabolism in obesity. The prevalence of obesity has led to an increase in the incidence of obesity-related glomerulopathy (ORG). This study aimed to identify the protective role of adiponectin in ORG.MethodsSmall-interfering RNA (siRNA) against the gene encoding adiponectin was transfected into podocytes. The oxidative stress level was determined using a fluorometric assay. Apoptosis was analyzed by flow cytometry. The expressions of podocyte markers and pyrin domain containing protein 3 (NLRP3) inflammasome-related proteins were measured by qRT-PCR, immunohistochemistry, and Western blot.ResultsPodocytes treated with palmitic acid (PA) showed downregulated expressions of podocyte markers, increased apoptosis, upregulated levels of NLRP3 inflammasome-related proteins, increased production of inflammatory cytokines (IL-18 and IL-1β), and induced activation of NF-κB as compared to the vehicle-treated controls. Decreased adiponectin expression was observed in the serum samples from high fat diet (HFD)-fed mice. Decreased podocin expression and upregulated NLRP3 expression were observed in the kidney samples from high fat diet (HFD)-fed mice. Treatment with adiponectin or the NLRP3 inflammasome inhibitor, MCC950, protected cultured podocytes against podocyte apoptosis and inflammation. Treatment with adiponectin protected mouse kidney tissues against decreased podocin expression and upregulated NLRP3 expression. The knockout of adiponectin gene by siRNA increased ROS production, resulting in the activation of NLRP3 inflammasome and the phosphorylation of NF-κB in podocytes. Pyrrolidine dithiocarbamate, an NF-κB inhibitor, prevented adiponectin from ameliorating FFA-induced podocyte injury and NLRP3 activation.ConclusionsOur study showed that adiponectin ameliorated PA-induced podocyte injury in vitro and HFD-induced injury in vivo via inhibiting the ROS/NF-κB/NLRP3 pathway. These data suggest the potential use of adiponectin for the prevention and treatment of ORG.

Dataset Information

Atheroprotective Mechanisms of Tilianin by Inhibiting Inflammation Through Down-Regulating NF-?B Pathway and Foam Cells Formation.

Publications

Atheroprotective Mechanisms of Tilianin by Inhibiting Inflammation Through Down-Regulating NF-κB Pathway and Foam Cells Formation.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets