Resveratrol Protects Murine Chondrogenic ATDC5 Cells Against LPS-Induced Inflammatory Injury Through Up-Regulating MiR-146b

Cellular Physiology and Biochemistry

Hui Jin¹ 

关键词: Resveratrol;    Osteoarthritis;    ATDC5 cell;    LPS;    MiR-146b;   

DOI  :  10.1159/000490141

学科分类：分子生物学，细胞生物学和基因

来源: S Karger AG

【 摘 要 】

Background/Aims Resveratrol (RSV) has been reported as a promising oral supplementation for osteoarthritis treatment, while the mechanism of its action is still unclear. The specific aim of this study is to decode one of the mechanisms by which RSV protects chondrocyte. Methods Mouse chondrogenic cell line ATDC5 was treated with 30 µM RSV for 24 h, and 10 µg/ml LPS for 12 h, after which cell viability, apoptosis, and the release of pro-inflammatory cytokines were assessed. The expression of miR-146b in ATDC5 cells was silenced by the specific inhibitor transfection, and then cell viability, apoptosis and inflammation were re-assessed. Results The IC50 value of LPS in ATDC5 cells was about 10.27 µg/ml. LPS with a dosage of 10 µg/ml repressed cell viability, induced apoptosis, and increased the release of IL-1β, IL-6 and TNF-α. RSV pre-treatment (30 µM) significantly alleviated LPS-induced apoptosis and inflammation. More importantly, miR-146b was up-regulated by RSV, and the protective functions of RSV on ATDC5 cells were attenuated by miR-146b silence. Further, NF-κB and p38MAPK pathways were activated by LPS, and were deactivated by RSV. Besides, RSV-induced the deactivation of NF-κB and p38MAPK pathways was reversed by miR-146b silence. Conclusions Our findings suggest that RSV protects ATDC5 cells from LPS-induced inflammatory and apoptotic injury via up-regulation of miR-146b and thereby deactivation of NF-κB and p38MAPK pathways.

【 授权许可】

CC BY-NC-ND