• Xirui Yang, Qi Zhang, Zhaomeng Gao, Chunyan Yu, and Lei Zhang.
• Department of Rheumatology and Immunology, Shengli Oilfield Central Hospital, Dongying 257000, Shandong, China.
• Biomed. Pharmacother. 2018 Mar 1; 99: 184-190.

AbstractBaicalin is a flavonoid extracted from Scutellaria baicalensis Georgi, with anti-inflammatory and anti-apoptotic activities. The objective of this study was to explore the effect and mechanism of baicalin on chondrocyte inflammatory response in OA. Different concentrations of IL-1β (0, 0.1, 2, 5 and 10 ng/mL) were used to simulate inflammatory injury in CHON-001 cells. The expression of miR-126 was altered by transfection with miR-126 mimic. Thereafter, cells were treated with baicalin, and cell viability, apoptosis, the expressions of apoptosis-related protein and pro-inflammatory factors were respectively detected using CCK-8 assay, flow cytometry, qRT-PCR and western blot analysis. We found that IL-1β induced a significantly inflammatory injury in CHON-001 cells. Baicalin alleviated IL-1β-induced inflammatory injury, as it increased cell viability, decreased cell apoptosis and repressed the production of IL-6, IL-8 and TNF-α. miR-126 was up-regulated by IL-1β treatment while was down-regulated by baicalin. More interestingly, the protective actions of baicalin on IL-1β-injured CHON-001 cells were partially eliminated by miR-126 overexpression. Further, NF-κB signaling pathway was activated by IL-1β, and deactivated by addition of baicalin. The deactivation of NF-κB signaling pathway induced by baicalin upon IL-1β exposure was recovered by miR-126 overexpression. In conclusion, this study demonstrated that baicalin protected CHON-001 cells against IL-1β-induced inflammatory injury possibly via down-regulation of miR-126 and thereby deactivation of NF-κB signaling pathway.Copyright © 2018 Elsevier Masson SAS. All rights reserved.

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