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ORIGINAL ARTICLE
Year : 2018  |  Volume : 11  |  Issue : 1  |  Page : 73-77

Autophagy plays a protective role in advanced glycation end products- induced apoptosis of chondrocytes via regulation of tumor necrosis factor-α , nuclear factor-κ B and reactive oxygen species


Orthopaedics Key Laboratory of Gansu Province, The Second Hospital of Lanzhou University, Lanzhou 730030, China

Correspondence Address:
Ya-Yi Xia
Orthopaedics Key Laboratory of Gansu Province, The Second Hospital of Lanzhou University, No. 82 Cuiyingmen, Chengguan District, Lanzhou 730030
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1995-7645.223577

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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- α (TNF- a ) and nuclear factor- κ B (NF- κ 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- α and NF- κ 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- α and NF- κ B expression, ROS accumulation and apoptosis; meanwhile, autophagy ameliorates the AGEs- induced adverse effects.


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