Abstract：Objective: To explore the effect of Platycodin D on cartilage tissue injury in knee osteoarthritis (KOA) rats by adjusting the adenosine monophosphate-activated protein kinase (AMPK)/PTEN induced putative kinase 1 (PINK1)/E3 ubiquitin ligase (Parkin) signaling pathway. Methods: Rats were divided into control (NC) group, model group, Platycodin D low-dose group (Platycodin D-L group), Platycodin D high-dose group (Platycodin D-H group), and Platycodin D-H+AMPK pathway inhibitor (Compound C) group, with 10 rats in each group, HE staining method was used to observe the morphological changes of rat cartilage tissue, and the Mankin score was performed. The reagent kit was used to detect the levels of oxidative damage markers SOD, MDA, and NO in the knee cartilage tissue of KOA rats in each group. The DCFH-DA probe was used to detect reactive oxygen species (ROS). The expression levels of inflammatory factors interleukin (IL)-6, tumor necrosis factor α (TNF-α), interleukin (IL)-1β, and monocyte chemoattractant protein 1 (MCP1) in cartilage tissues of each group were detected by ELISA. The TUNEL staining method was used to detect cell apoptosis in the knee cartilage tissue of KOA rats in each group. Western blot was used to detect Caspase 3, Bcl-2 family K protein (Bak), and AMPK/PINK1/Parkin pathway related proteins in cartilage tissue. Results: Compared with the NC group, in the Model group, the rat knee joint cartilage tissue cells were arranged disorderly, with severe cartilage damage. The Mankin score, levels of MDA, NO, ROS, IL-6, TNF-α, IL-1β, and MCP1, cell apoptosis rate, and protein expression levels of Caspase3 and Bak were significantly increased (P<0.05), while the SOD level and protein expression levels of p-AMPK, p-PINK1, and p-Parkin were significantly decreased (P<0.05). Compared with the Model group, in the Platycodin D-L and Platycodin D-H groups, the knee joint cartilage tissue damage in rats was alleviated. The Mankin score, levels of MDA, NO, ROS, IL-6, TNF-α, IL-1β, and MCP1, cell apoptosis rate, and protein expression levels of Caspase3 and Bak were significantly decreased (P<0.05), while the SOD level and protein expression levels of p-AMPK, p-PINK1, and p-Parkin were significantly increased (P<0.05). In the Platycodin D-H + Compound C group, the alleviating effect of Platycodin D on cartilage tissue damage was reversed (P<0.05). Conclusion: Platycodin D may alleviate cartilage tissue injury in KOA rats by adjusting AMPK/PINK1/Parkin signaling pathway.
王平, 柳玉兵. 桔梗皂苷D调节AMPK/PINK1/Parkin信号通路对膝骨关节炎大鼠软骨组织损伤的影响[J]. 河北医学, 2025, 31(8): 1233-1239.
WANG Ping, LIU Yubing. Effects of Platycodin D on Cartilage Tissue Injury in Knee Osteoarthritis Rats by Adjusting the AMPK/PINK1/Parkin Signaling Pathway. HeBei Med, 2025, 31(8): 1233-1239.
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2025, Vol. 31 
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