Acetyl-L-Carnitine Inhibits Neuronal Ferroptosis and Promotes Spinal Cord Injury Repair by Activating the Nrf2/GPX4 Pathway
XI Huilin1,2, WU Jiajun1, TIAN Chunping1, BAI Xinyue1, WANG Qingyan1, HE Mengze1, YANG Yanling1*
After SCI (spinal cord injury), a series of pathological processes occur, such as the serious neu ronal ferroptosis, which is one of the important factors leading to functional disorders after SCI. Therefore, this ex periment is designed to explore the effect and mechanism of ALC (acetyl-L-carnitine) on neuronal ferroptosis and functional repair after SCI. The HI-0400 spinal cord impactor was used to impact the T10 segment of the spinal cord of rats to establish an acute SCI model in rats. The BBB scale was used to evaluate the motor function, HE staining was used to observe the morphological changes of the spinal cord tissue, and Nissl staining was used to observe the survival of spinal cord neurons. By examining the expression levels of molecules related to the Nrf2/GPX4 signaling pathway and ferroptosis marker proteins, and evaluating ferroptosis indicators (MDA, GSH, Fe²⁺) in PC12 cells in vi tro, the effects of ALC were investigated. The results showed that ALC could significantly improve motor function and spinal cord tissue morphology in SCI rats. Its mechanism is related to upregulating neuronal Nrf2 expression, thereby enhancing GPX4 activity and improving GSH content, while simultaneously reducing lipid peroxidation MDA and Fe²⁺ levels. The Nrf2 inhibitor Brusatol could reverse the effect of ALC. ALC promotes the functional recovery in SCI rats, ALC inhibits neuronal ferroptosis through the Nrf2/GPX4 signaling pathway.
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