Liu Xinyue, Han Yan, Tang Xinhui, Ren Yun, Gao Weiqi, Li Yongai, Xue Yuchen, Li Xinghua, Suo Yuping
The Gynecology Department of Shanxi Provincial People Hospital, Shanxi Medical University, No. 29, Shuangta East Street, Yingze District, Taiyuan, 030001, China.
Changzhi People's HospitalAffiliated to Changzhi Medical College, 502 Changxing Zhong Road, Changzhi, 046000, China.
Naunyn Schmiedebergs Arch Pharmacol. 2025 Jul 24. doi: 10.1007/s00210-025-04430-2.
Cisplatin (CIS), a widely used platinum-based chemotherapeutic agent, often induces ovarian toxicity that severely threatens female reproductive health. Paeonol (PAE), a bioactive compound found in peony, exhibits multiple pharmacological activities. This study investigates the multitarget protective mechanisms of PAE against cisplatin-induced premature ovarian failure (POF) using network pharmacology, molecular docking, and molecular dynamics simulations. We identified 93 potential targets of PAE and discovered significant activation of inflammation-related pathways, particularly the IL-17 and TNF signaling pathways. Protein-protein interaction (PPI) network analysis pinpointed ten core hub genes, including NFKB1, TNF, and IL6. Molecular docking and dynamics simulations confirmed PAE's stable binding to key targets like IL-6 and TNFα. In vitro experiments demonstrated that PAE significantly reduced oxidative stress markers (ROS, MDA, and LDH) and restored SOD activity in cisplatin-damaged KGN cells, while downregulating pro-inflammatory factors (TNFα and IL-6). Mechanistic studies revealed that PAE protects ovaries by synergistically regulating the IL-17 signaling pathway to inhibit POF. This research elucidates PAE's ovarian protective mechanisms from a multi-omics perspective, offering new evidence for natural compound-based POF prevention and treatment strategies.
顺铂(CIS)是一种广泛使用的铂类化疗药物,常诱发卵巢毒性,严重威胁女性生殖健康。丹皮酚(PAE)是从牡丹中发现的一种生物活性化合物,具有多种药理活性。本研究采用网络药理学、分子对接和分子动力学模拟方法,探讨PAE对顺铂诱导的卵巢早衰(POF)的多靶点保护机制。我们确定了PAE的93个潜在靶点,并发现炎症相关通路,特别是IL-17和TNF信号通路有显著激活。蛋白质-蛋白质相互作用(PPI)网络分析确定了10个核心枢纽基因,包括NFKB1、TNF和IL6。分子对接和动力学模拟证实了PAE与IL-6和TNFα等关键靶点的稳定结合。体外实验表明,PAE显著降低了顺铂损伤的KGN细胞中的氧化应激标志物(ROS、MDA和LDH),并恢复了SOD活性,同时下调了促炎因子(TNFα和IL-6)。机制研究表明,PAE通过协同调节IL-17信号通路来抑制POF,从而保护卵巢。本研究从多组学角度阐明了PAE的卵巢保护机制,为基于天然化合物的POF预防和治疗策略提供了新的证据。