Interplay between oxidative stress and autophagy function and its role in inflammatory cytokine expression induced by palmitate in skeletal muscle cells
| Autor: | Asie Sadeghi, Reza Meshkani, Maryam Shabani, Samira Alizadeh |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Immunology Palmitates Inflammation medicine.disease_cause Biochemistry Cell Line Proinflammatory cytokine Mice 03 medical and health sciences 0302 clinical medicine Sequestosome-1 Protein Autophagy medicine Animals Immunology and Allergy Muscle Skeletal Molecular Biology Sirolimus chemistry.chemical_classification Reactive oxygen species Interleukin-6 Tumor Necrosis Factor-alpha Chemistry Adenine Skeletal muscle Chloroquine Free Radical Scavengers Hematology Hypoxia (medical) Acetylcysteine Cell biology Oxidative Stress 030104 developmental biology medicine.anatomical_structure 030220 oncology & carcinogenesis Cytokines medicine.symptom Reactive Oxygen Species Microtubule-Associated Proteins C2C12 Oxidative stress |
| Zdroj: | Cytokine. 125:154835 |
| ISSN: | 1043-4666 |
| Popis: | Autophagy is a cellular process activated in response to various stresses such as starvation, hypoxia, and oxidative stress. Autophagy was reported to modulate the inflammatory pathways. However, whether autophagy is involved in regulation of palmitate-induced inflammation of skeletal muscle C2C12 cells is still unknown. The present study aimed to investigate the autophagic pathway in C2C12 cells treated with 0.5 mM palmitate. The results showed that the protein levels of LC3BII and P62 were increased in C2C12 cells after 12 h palmitate treatment. Besides, inhibition of autophagy by chloroquine or 3-methyladenin and its activation by rapamycin were associated with elevated mRNA and protein levels of IL-6 and TNF-α inflammatory cytokines in C2C12 cells. To study the mechanism by which autophagy impairment leads to activation of inflammatory responses, reactive oxygen species (ROS) levels in palmitate-treated cells were measured. The results showed that while palmitate stimulates ROS production, pretreatment of the cells with N-acetyl cysteine (NAC), a ROS scavenger, reduced inflammatory responses and also improved LC3-BII and P62 protein in the C2C12 cells exposed to palmitate. These findings suggest that palmitate-induced defect of autophagic flux leads to elevated inflammatory cytokine expression in the skeletal muscle cells by regulating the oxidative stress process. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect