Autophagy plays a protective role in advanced glycation end products-induced apoptosis of chondrocytes via regulation of tumor necrosis factor-
Asian Pacific Journal of Tropical Medicine
;
(12): 73-77, 2018.
Artigo
em Chinês
| WPRIM
| ID: wpr-972506
ABSTRACT
Objective:
To study the adverse effects of advanced glycation end products (AGEs) on chondrocytes and the role of autophagy in this process.Methods:
Chondrocytes were harvested from the human articular cartilage tissues in surgery. AGEs were administered during chondrocytes culture. The rapamycin was used to induce autophagy. The cell viability was determined by 3-[4,5-dimethylthiazol2-yl]-2,5-diphenyl tetrazolium bromide (MTT) assay. The expression of tumor necrosis factor-? (TNF-?) and nuclear factor-?B (NF-?B) was detected by quantitative real-time polymerase chain reaction. The reactive oxygen species (ROS) production and apoptosis of the chondrocytes were determined by fluorescent probe and flow cytometer, respectively.Results:
The chondrocytes viability was significantly reduced after 12 h incubation with AGEs (P<0.01)). In contrast, rapamycin pretreatment increased the chondrocytes viability through autophagy. AGEs increased TNF-? and NF-?B mRNA expression of chondrocytes and autophagy receded or proceeded the change. AGEs increased intracellular ROS accumulation and autophagy reversed the change. AGEs accelerated chondrocytes apoptosis and autophagy suspended apoptosis.Conclusions:
Accumulation of AGEs may have an adverse role for chondrocytes by increasing TNF-? and NF-?B expression, ROS accumulation and apoptosis; meanwhile, autophagy ameliorates the AGEs-induced adverse effects.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Idioma:
Chinês
Revista:
Asian Pacific Journal of Tropical Medicine
Ano de publicação:
2018
Tipo de documento:
Artigo
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