Sulforaphane modulates CX3CL1/CX3CR1 axis and inflammation in palmitic acid-induced cell injury in C2C12 skeletal muscle
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ORIGINAL ARTICLE
Sulforaphane modulates CX3CL1/CX3CR1 axis and inflammation in palmitic acid‑induced cell injury in C2C12 skeletal muscle cells Yousef Faridvand1,2 · Parinaz Haddadi3 · Hamid Reza Nejabati2 · Samad Ghaffari1 · Elham Zamani‑Gharehchamani3 · Samira Nozari4,5 · Mohammad Nouri1,5,6 · Ahmadreza Jodati1 Received: 18 April 2020 / Accepted: 29 September 2020 © Springer Nature B.V. 2020
Abstract 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 obesityassociated disorders in skeletal muscle cells. Keywords Sulforaphane · CX3CL1 · Palmitic acid · ROS · C2C12
Introduction
* Mohammad Nouri [email protected] * Ahmadreza Jodati [email protected] 1
Cardiovascular Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
2
Department of Biochemistry and Clinical Laboratories, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran
3
Department of Biochemistry, Faculty of Sciences, Tabriz University, Tabriz, Iran
4
Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran
5
Stem Cells Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
6
Stem Cell and Regenerative Medicine (SCARM) Institute, Tabriz University of Medical Sciences, Tabriz, Iran
Obesity dramatically has increased risk for diseases such as dyslipidemia, atherosclerosis, hypertension, and diabetes [1]. Obesity is characterized by an inflammatory state, insulin resistance, and metabolic disorders, which increase the pathological complication of diabetes and cardiovascular disease [2, 3]. Obesity raises the level of free fatty acids (FFAs) and its derivatives, which induce low-grade inflammation in the tissues such as live
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