| Objective To investigate the effect of atractylenolide I (AT-I) on the inflammatory injury of articular chondrocytes induced by interleukin-1β (IL-1β). Methods Human articular chondrocytes were from Wuhan Punosai Life Technology Co., LTD. The experiment was divided into six groups: control group (untreat), model group (10 ng/mL IL-1β), AT-I-L group (25 μmol/L), AT-I-M group (50 μmol/L), AT-I-H group (100 μmol/L ), and AT-I-H+740 Y-P group (100 μmol/L AT-I and 50 μg/mL 740 Y-P phosphatidylinositol 3-kinase (PI3K) activator). CCK-8 method and flow cytometry were applied to determine the proliferation and apoptosis, respectively. ELISA method was applied to measure the level of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the supernatant. Western blotting was applied to detect the expression of PI3K/protein Kinase B (AKT)/Nuclear factor-κB (NF-κB) pathway related proteins. Results Compared to those in the control group, OD450 values (24 h, 48 h) in the model group reduced (P<0.05), the TNF-α, IL-6 expression, apoptosis rate, and PI3K/AKT/NF-κB pathway protein expression increased obviously (P<0.05). Compared with the model group, the AT-I-L group showed no obvious differences in OD450 values (24 h, 48 h), TNF-α, IL-6 expression, apoptosis rate, and PI3K/AKT/NF-κB pathway protein expression (P>0.05). OD450 values (24 h, 48 h) in the AT-I-M and AT-I-H groups increased (P<0.05), and TNF-α, IL-6 expression, apoptosis rate, and PI3K/AKT/NF-κB pathway protein expression decreased (P<0.05). Compared to those in the AT-I-H group, OD450 values (24 h, 48 h) in the AT-I-H+740 Y-P group reduced (P<0.05), TNF-α and IL-6 expression, cell apoptosis rate, and PI3K/AKT/NF-κB pathway protein expression increased (P<0.05). Conclusion AT-I improves the inflammatory injury of articular chondrocytes induced by IL-1β. The possible mechanism is to promote chondrocyte proliferation and to inhibit inflammatory response, apoptosis, and PI3K/AKT/NF-κB pathway. |