文献类型：期刊文献

英文题名：Ginkgolide B inhibits ferroptosis in PC12 cells and ameliorates the oxidative stress in spinal cord injury through activating Nrf2 signaling pathway

作者：She, Wei[1,2];Ma, Wenji[3];Zhang, Tongtong[2];Wu, Xunian[4];Li, Jianfu[2];Li, Xingyong[1,2]

第一作者：She, Wei

通信作者：Li, XY[1]

机构：[1]Gansu Univ Chinese Med, Lanzhou 730000, Gansu, Peoples R China;[2]Gansu Prov Hosp, Dept Orthopaed Surg, Donggang West Rd, Lanzhou 730000, Gansu, Peoples R China;[3]Lanzhou Univ, Hosp 1, Dept Orthopaed Surg, Lanzhou 730000, Gansu, Peoples R China;[4]Second People Hosp Zhangye, Dept Orthopaed Surg, Zhangye 734000, Gansu, Peoples R China

第一机构：甘肃中医药大学

通信机构：[1]corresponding author), Gansu Prov Hosp, Dept Orthopaed Surg, Donggang West Rd, Lanzhou 730000, Gansu, Peoples R China.

年份：2025

卷号：158

期号：3

起止页码：199

外文期刊名：JOURNAL OF PHARMACOLOGICAL SCIENCES

收录：;Scopus(收录号：2-s2.0-105004270411);WOS:【SCI-EXPANDED(收录号:WOS:001487182500001)】；

语种：英文

外文关键词：Ginkgolide B; Spinal cord injury; Ferroptosis; Nrf2; GPX4

摘要：Spinal cord injury (SCI) commonly leads to loss of motor and sensory function and results in huge socioeconomic burden, and it triggers numerous secondary pathological events, including oxidative stress and ferroptosis. This study investigates the therapeutic potential of Ginkgolide B (GB), a neuroprotective compound derived from Ginkgo biloba, in mitigating SCI by targeting on ferroptosis. By using Erastin-induced ferroptosis in PC12 cells and a rat contusion SCI model, the present study demonstrated that GB significantly improved locomotor recovery, reduced neuronal loss, and attenuated histopathological damage. Mechanistically, GB suppressed ferroptosis markers, including elevated iron content, lipid peroxidation, and ACSL4, while restoring the expression of GPX4 and xCT. Crucially, GB enhanced nuclear translocation of Nrf2, upregulating downstream antioxidants and ferroptosis-related genes (HO-1 and NQO1). Notably, the functions of GB were abolished after utilization of Nrf2 signaling inhibitor ML385 which revealed the role of GB on recovery of SCI was highly related to the activation of Nrf2 signaling. These findings reveal that GB alleviates SCI by inhibiting ferroptosis through Nrf2 activation, positioning it as a promising therapeutic agent. This study elucidates a novel mechanism linking Nrf2 signaling to ferroptosis suppression in SCI and provides a translational framework for repurposing GB in SCI treatment.