This study aimed to explore the mechanism of hepatoprotective effect of Platycodon grandiflorus polysaccharides (PGPS_t) on LPS/D-galactose (D-GalN)-induced acute liver injury in mice. The pathological changes of liver tissue were observed by H&E stain. The results showed that the structure of hepatocytes in the model group was destroyed obviously, and that in 200 mg/kg PGPS_t group was improved, which indicated that PGPS_t could reduce the damage of hepatocytes. Then, indicators of oxidative stress, inflammatory cytokines and apoptosis were detected. The results showed that PGPS_t significantly reduced the activities of AST, ALT and SOD. PGPS_t increased the expression of GSH, and decreased the level of MDA, IL-6, IL-1β and TNF-α. PGPS_t can inhibit hepatocyte apoptosis, which might be related to down-regulation of cleaved-caspase 3 and Bax, and up-regulation of Bcl-2. In addition, Western blot analyses revealed that PGPS_t suppressed the protein expression of TRL4, p-P38 and NF-κB p65. PGPS_t exhibited protective effects on LPS/D-GalN-induced acute liver injury in mice. Conclusion, the results demonstrated that PGPS_t is a potential therapeutic drug by alleviating oxidative stress, reducing inflammatory cytokines and enhancing the expression of anti-apoptotic proteins that could be used for the treatment of some acute liver injury in the future.

本研究旨在探讨桔梗多糖（PGPS _t）对LPS / D-半乳糖（D-GalN）诱导的小鼠急性肝损伤的肝保护作用机制。H＆E染色观察肝组织的病理变化。结果表明，模型组肝细胞结构明显破坏，200 mg / kg PGPS _t组改善，提示PGPS _t可减轻肝细胞损伤。然后，检测氧化应激，炎性细胞因子和细胞凋亡的指标。结果表明，PGPS _t显着降低了AST，ALT和SOD的活性。PGPS _Ť增加GSH的表达，降低MDA，IL-6，IL-1β和TNF-α的水平。PGPS _t可以抑制肝细胞凋亡，这可能与Caspase 3和Bax的下调以及Bcl-2的上调有关。此外，蛋白质印迹分析表明，PGPS _t抑制了TRL4，p-P38和NF-κBp65的蛋白表达。PGPS _t对LPS / D-GalN诱导的小鼠急性肝损伤具有保护作用。结论，结果表明，PGPS _t是减轻氧化应激，减少炎症细胞因子和增强抗凋亡蛋白表达的潜在治疗药物，可用于将来治疗某些急性肝损伤。