Sulforaphane modulates CX3CL1/CX3CR1 axis and inflammation in palmitic acid-induced cell injury in C2C12 skeletal muscle cells

被引:0
作者
Yousef Faridvand
Parinaz Haddadi
Hamid Reza Nejabati
Samad Ghaffari
Elham Zamani-Gharehchamani
Samira Nozari
Mohammad Nouri
Ahmadreza Jodati
机构
[1] Tabriz University of Medical Sciences,Cardiovascular Research Center
[2] Tabriz University of Medical Sciences,Department of Biochemistry and Clinical Laboratories, Faculty of Medicine
[3] Tabriz University,Department of Biochemistry, Faculty of Sciences
[4] Tabriz University of Medical Sciences,Student Research Committee
[5] Tabriz University of Medical Sciences,Stem Cells Research Center
[6] Tabriz University of Medical Sciences,Stem Cell and Regenerative Medicine (SCARM) Institute
来源
Molecular Biology Reports | 2020年 / 47卷
关键词
Sulforaphane; CX3CL1; Palmitic acid; ROS; C2C12;
D O I
暂无
中图分类号
学科分类号
摘要
Studies have shown that sulforaphane (SFN) has potent anti-inflammatory and free radical scavenging effects on obesity and associated disorder such as diabetes, polycystic ovary syndrome, and metabolic syndrome. fractalkine (CX3CL1) and its receptor, CX3CR1, play an important role in muscle metabolism by improving insulin-sensitizing effects. Here, in this study we examined the SFN effect on CX3CL1 and its receptor, CX3CR1, in C2C12 myotubes in palmitic acid (PA)-induced oxidative stress and inflammation. The results showed that PA (750 μM) evoked lipotoxicity as a reduction in cell viability, increased IL-6 and TNF-α expression, and enhanced reactive oxygen species (ROS). However, SFN pretreatment attenuated the levels of, IL-6 and TNF-α in C2C12 myotubes exposure to PA. Moreover, SFN pretreatment up-regulated nuclear factor erythroid related factor 2 (Nrf2) /heme oxygenase-1(HO-1) pathway protein in C2C12 cells as indicated by a decrease in ROS levels. Interestingly, PA also caused an increase in CX3CL1 and CX3CR1 expression that SFN abrogated it. We also found the protective effect of SFN agonist PA-induced lipotoxicity with promotes in UCP3 gene expression in C2C12 cells. Collectively, these findings suggest that SFN hampers the PA-induced inflammation in C2C12 cells by modulation of the Nrf2/HO-1 pathway and CX3CL1/CX3CR1 axis and may propose a new therapeutic approach to protect against obesity-associated disorders in skeletal muscle cells.
引用
收藏
页码:7971 / 7977
页数:6
相关论文
共 238 条
[1]  
DeBoer MD(2013)Obesity, systemic inflammation, and increased risk for cardiovascular disease and diabetes among adolescents: a need for screening tools to target interventions Nutrition 29 379-386
[2]  
Mathieu P(2010)Obesity, inflammation, and cardiovascular risk Clin Pharmacol Ther 87 407-416
[3]  
Lemieux I(2014)Oxidative stress and inflammation in obesity, diabetes, hypertension, and related cardiometabolic complications Oxid Med Cell Longev 2014 506948-1618
[4]  
Despres JP(2015)Intermuscular and perimuscular fat expansion in obesity correlates with skeletal muscle T cell and macrophage infiltration and insulin resistance Int J Obes (Lond) 39 1607-13
[5]  
Ndisang JF(2019)The role of skeletal muscle Akt in the regulation of muscle mass and glucose homeostasis Mol Metab 28 1-267
[6]  
Vannacci A(2014)Insulin resistance is associated with MCP1-mediated macrophage accumulation in skeletal muscle in mice and humans PLoS ONE 9 e34976-35
[7]  
Rastogi S(2012)Mechanisms underlying skeletal muscle insulin resistance induced by fatty acids: importance of the mitochondrial function Lipids Health Dis 11 30-1518
[8]  
Khan IM(2014)Identification of human exercise-induced myokines using secretome analysis Physiol Genomics 46 256-425
[9]  
Perrard XY(2014)The fractalkine/Cx3CR1 system is implicated in the development of metabolic visceral adipose tissue inflammation in obesity Brain Behav Immunity 38 25-304
[10]  
Brunner G(2011)Fractalkine is a novel human adipochemokine associated with type 2 diabetes Diabetes 60 1512-17795