Tanshinone IIA Promotes Functional Recovery After Spinal Cord Injury by Inhibiting Neuron and Oligodendrocyte Ferroptosis Through the GPX4/ACSL4 Axis

被引：0

作者：

Luchun Xu ^{[1
]}

Guozheng Jiang ^{[1
]}

Shuyin Tan ^{[1
]}

Yukun Ma ^{[1
]}

Jiawei Song ^{[1
]}

Yushan Gao ^{[2
]}

Guanlong Wang ^{[1
]}

Jiaojiao Fan ^{[1
]}

Yongdong Yang ^{[1
]}

Xing Yu ^{[1
]}

机构：

[1] Beijing University of Chinese Medicine,Department of Orthopedics, Dongzhimen Hospital

[2] Beijing University of Chinese Medicine,School of Traditional Chinese Medicine

来源：

Neurochemical Research | 2025年 / 50卷 / 3期

关键词：

Tanshinone IIA; Spinal cord injury; Ferroptosis; GPX4; ACSL4;

D O I：

10.1007/s11064-025-04414-x

中图分类号：

学科分类号：

摘要：

Spinal cord injury (SCI) induces severe functional impairments and involves intricate secondary injury mechanisms. Tanshinone IIA (TIIA), a key bioactive component of Salvia miltiorrhiza, exhibits neuroprotective potential, yet its role in ferroptosis regulation post-SCI remains undefined. This study explored the protective effects and underlying mechanisms of TIIA in SCI. In a rat SCI model, TIIA markedly enhanced hind limb motor function and preserved histopathological integrity while mitigating mitochondrial damage, ferroptosis, and oxidative stress. TIIA attenuated ferroptosis by reducing reactive oxygen species (ROS), malondialdehyde (MDA), and acyl-CoA synthetase long-chain family member 4 (ACSL4) while elevating glutathione (GSH), superoxide dismutase (SOD), and glutathione peroxidase 4 (GPX4) levels. Mechanistically, TIIA suppressed ferroptosis through modulation of the GPX4/ACSL4 axis. The ferroptosis inducer RSL3 abrogated these protective effects, further validating this mechanism. These findings highlight the therapeutic potential of TIIA in SCI by targeting the GPX4/ACSL4 pathway to attenuate ferroptosis and promote functional recovery.

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