基于网络药理学、分子对接和实验验证探讨牡丹皮多糖治疗非酒精性脂肪肝炎机制研究
Exploring the Mechanism of Polysaccharide of Moutan Cortex in Treating Non-Alcoholic Steatohepatitis Based on Network Pharmacology, Molecular Docking, and Experimental Verification
DOI: 10.12677/acm.2026.1672681, PDF,   
作者: 罗家骏*：深圳市龙华区人民医院同胜社康服务中心中医全科，广东 深圳；邓 旋：江西省丰城市桥东镇中心卫生院中医内科，江西 宜春；何 旭, Abid Muhammad：大连医科大学中西医结合学院，辽宁 大连；余佳发#：广东省华立技师学院(江门校区)医务室，广东 江门
关键词: 牡丹皮多糖；非酒精性脂肪性肝炎；网络药理学；分子对接；Polysaccharide of Moutan Cortex； Non-Alcoholic Steatohepatitis； Network Pharmacology； Molecular Docking
摘要: 目的：探究牡丹皮多糖治疗非酒精性脂肪性肝炎(NASH)的潜在靶点。方法：通过成分鉴定、网络药理学和分子对接分析牡丹皮多糖的作用机制，结合细胞实验、q-PCR及油红O染色验证其疗效。结果：牡丹皮多糖的关键靶点为AKT1、PI3KR1、MMP9，可能通过调控缺氧反应、凋亡及PI3K/AKT、AGE-RAGE、MAPK等信号通路改善NASH。分子对接显示其与靶蛋白结合良好，实验证实其可显著减轻脂肪变性和脂毒性损伤。结论：牡丹皮多糖通过调节PI3K/AKT通路治疗NASH，为NASH治疗提供新策略。
Abstract: Objective: To explore the potential targets of Polysaccharide of Moutan Cortex in the treatment of non-alcoholic steatohepatitis (NASH). Methods: The mechanism of action of Polysaccharide of Moutan Cortex was analyzed through component identification, network pharmacology, and molecular docking. The efficacy was verified through cell experiments, q-PCR, and Oil Red O staining. Results: The key targets of Polysaccharide of Moutan Cortex are AKT1, PI3KR1, and MMP9, which may improve NASH by regulating hypoxia response, apoptosis, and signaling pathways such as PI3K/Akt, AGE-RAGE, and MAPK. Molecular docking showed good binding with target proteins, and experiments confirmed that it can significantly reduce steatosis and lipotoxic damage. Conclusion: Polysaccharide of Moutan Cortex treat NASH by regulating the PI3K/AKT pathway, providing a new strategy for the treatment of NASH.
文章引用：罗家骏, 邓旋, 何旭, Abid Muhammad, 余佳发. 基于网络药理学、分子对接和实验验证探讨牡丹皮多糖治疗非酒精性脂肪肝炎机制研究[J]. 临床医学进展, 2026, 16(7): 1600-1609. https://doi.org/10.12677/acm.2026.1672681

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