| Objective To investigate the impacts of salidroside (Sal) on inflammatory injury of articular chondrocytes. Methods Experimental group: Human articular chondrocytes were separated into control group (conventional culture), IL-1β group (50 ng/mL), Sal-2μmol/L, Sal-4μmol/L, Sal-8μmol/L groups, and Sal+GW0742 group (8μmol/L Sal+4μmol/L CCL2-CCR2 signal axis activator GW0742). Human articular chondrocytes were treated with 50ng/mL IL-1β to establish the injury model of articular chondrocytes. MTT method was applied to detect the toxicity of Sal and GW0742 on articular chondrocytes. Plate cloning experiments and flow cytometry were applied to detect cell proliferation and apoptosis. ELISA was applied to detect the levels of inflammation related factors (IL-10, TNF-α, IL-6). QRT-PCR was applied to detect the expression of CCL2 and CCR2 mRNA in cells. Western blot was applied to detect the expression of proliferation and apoptosis related proteins (PCNA, Cleaved Caspase-3) and CCL2-CCR2 signaling axis proteins. Results Compared to the control group, the number of colony formation, the expression of IL-10, and PCNA reduced in the IL-1β group, the apoptosis rate, the expression of TNF-α, IL-6, CCL2, CCR2 mRNA, and the expression of Cleaved Caspase-3, CCL2, and CCR2 increased (P<0.05). Compared to the IL-1β group, the number of colony formation, the expression of IL-10, and PCNA in the Sal-2μmol/L, Sal-4μmol/L, and Sal-8μmol/L groups increased sequentially, the apoptosis rate, the expression of TNF-α, IL-6, CCL2, CCR2 mRNA, and the expression of Cleaved Caspase-3, CCL2, and CCR2 decreased sequentially (P<0.05). CCL2-CCR2 signaling pathway activator GW0742 was able to weaken the protective effect of Sal on IL-1β-induced inflammatory injury of articular chondrocytes (P<0.05). Conclusion Sal may inhibit IL-1β-induced apoptosis and inflammatory response of articular chondrocytes by inhibiting the CCL2-CCR2 pathway. |