Objective To investigate the effect of Erianin on inflammatory injury of articular chondrocytes by regulating the C-C motif chemokine ligand 2 (CCL2)/C-C motif chemokine receptor 2 (CCR2) axis. Methods Human articular chondrocytes were grouped into control group (normal culture), LPS group, low (10nmol/L), medium (25nmol/L), and high (50nmol/L) dose groups, pcDNA group (transfected with pcDNA3.1), and pcDNA-CCL2 group (transfected with pcDNA3.1 CCL2). Real-time fluorescence quantitative PCR (qRT-PCR) was applied to detect the expression levels of CCL2 and CCR2 mRNA in cells. MTT assay, plate cloning assay, and flow cytometry were applied to detect cell proliferation and apoptosis, respectively. qRT-PCR and ELISA were applied to detect levels of IL-6, IL-1β, and TNF-α. Western blotting was applied to detect the expressions of proliferating cell nuclear antigen (PCNA), anti apoptotic factor B cell lymphoma protein 2 (Bcl-2), Bcl-2 associated X protein (Bax), and CCL2/CCR2 pathway protein in cells. Results Compared to those in the control group, the cell apoptosis rate, IL-6, IL-1β, TNF-α mRNA expression levels and contents, CCL2, CCR2 mRNA, and Bax, CCL2, and CCR2 protein expression levels obvious increased in the LPS group, and the OD490 value, colony formation number, and PCNA and Bcl-2 protein expression levels decreased (P<0.05). Compared to those in the LPS group, the cell apoptosis rate, IL-6, IL-1β, TNF-α mRNA expression levels and contents, CCL2, CCR2 mRNA, and Bax, CCL2, and CCR2 protein expression levels obvious decreased in the the low, medium, and high dose Erianin groups, and the OD490 value, colony formation number, and PCNA and Bcl-2 protein expression levels increased (P<0.05). Overexpression of CCL2 weakened the effect of Erianin on LPS-induced articular chondrocytes (P<0.05). Conclusion Erianin inhibits LPS-induced apoptosis and inflammatory response of articular chondrocytes. The mechanism may be related to the inhibition of CCL2/CCR2 pathway. |