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已发表论文
芹菜素通过促进线粒体自噬抑制实验性脊髓损伤大鼠的 NLRP3 炎性小体激活和细胞焦亡并促进功能恢复
Authors Wu Z, Fang Y , Dong Y, Qin Y , Liu A , Han T, Song P, Shen C
Received 24 June 2025
Accepted for publication 26 September 2025
Published 8 October 2025 Volume 2025:18 Pages 13965—13984
DOI https://doi.org/10.2147/JIR.S549251
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Dr Adam Bachstetter
Zuomeng Wu,1,2,* Yunxiao Fang,1,2,* Yixiang Dong,1,2 Yue Qin,1,2 Ao Liu,1,2 Tianyu Han,1,2 Peiwen Song,1,2 Cailiang Shen1– 3
1Department of Orthopedics (Spinal Surgery), The First Affiliated Hospital of Anhui Medical University, Hefei, 230032, People’s Republic of China; 2Laboratory of Spinal and Spinal Cord Injury Regeneration and Repair, The First Affiliated Hospital of Anhui Medical University, Hefei, 230032, People’s Republic of China; 3Anhui Province Research Center for the Clinical Application of Digital Medical Technology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, 230022, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Cailiang Shen, Email shencailiang@ahmu.edu.cn
Background: Secondary damage following spinal cord injury (SCI) is closely associated with pyroptosis and mitochondrial dysfunction. Apigenin (API), a natural flavonoid, possesses notable anti-inflammatory and antioxidant properties. However, whether API can inhibit microglial pyroptosis via the mitophagy pathway, thereby exerting neuroprotective effects, remains unclear. This study aimed to elucidate the mechanism by which API mitigates post-SCI inflammatory responses through modulation of the mitophagy-NLRP3 axis.
Methods: Neurological recovery was assessed using the Basso, Beattie, and Bresnahan scale, neuroelectrophysiological recordings, and histological analyses. The effects of API on NLRP3 inflammasome activation, reactive oxygen species (ROS) generation, and mitochondrial membrane potential were assessed using ELISA, quantitative PCR, immunofluorescence, and JC-1 staining.
Results: API significantly improved locomotor function in SCI rats, reduced scar formation, and promoted axonal regeneration. Mechanistically, API downregulated NLRP3/ gasdermin D expression in microglia, reduced the release of inflammatory factors, and enhanced mitophagy. Notably, the protective effects of API were reversed by Mdivi-1 and mimicked by Urolithin A, confirming that mitophagy is the primary mechanism mediating API’s anti-pyroptotic effects.
Conclusion: API attenuates microglial pyroptosis and facilitates SCI repair by enhancing mitophagy-mediated clearance of damaged mitochondria and suppressing activation of the ROS/NLRP3 inflammasome pathway in rats. These findings provide important preclinical evidence supporting the development of multi-target neuroprotective strategies derived from natural compounds.
Plain Language Summary: API effectively suppresses NLRP3 inflammasome activation and mitigates microglial pyroptosis.API enhances mitophagy in microglia following SCI.API inhibits pyroptosis through mitophagy-mediated regulation of NLRP3 activation.API significantly promotes locomotor recovery and neural regeneration in spinal cord-injured rats.
Keywords: spinal cord injury, apigenin, mitophagy, pyroptosis
1Department of Orthopedics (Spinal Surgery), The First Affiliated Hospital of Anhui Medical University, Hefei, 230032, People’s Republic of China; 2Laboratory of Spinal and Spinal Cord Injury Regeneration and Repair, The First Affiliated Hospital of Anhui Medical University, Hefei, 230032, People’s Republic of China; 3Anhui Province Research Center for the Clinical Application of Digital Medical Technology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, 230022, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Cailiang Shen, Email shencailiang@ahmu.edu.cn
Background: Secondary damage following spinal cord injury (SCI) is closely associated with pyroptosis and mitochondrial dysfunction. Apigenin (API), a natural flavonoid, possesses notable anti-inflammatory and antioxidant properties. However, whether API can inhibit microglial pyroptosis via the mitophagy pathway, thereby exerting neuroprotective effects, remains unclear. This study aimed to elucidate the mechanism by which API mitigates post-SCI inflammatory responses through modulation of the mitophagy-NLRP3 axis.
Methods: Neurological recovery was assessed using the Basso, Beattie, and Bresnahan scale, neuroelectrophysiological recordings, and histological analyses. The effects of API on NLRP3 inflammasome activation, reactive oxygen species (ROS) generation, and mitochondrial membrane potential were assessed using ELISA, quantitative PCR, immunofluorescence, and JC-1 staining.
Results: API significantly improved locomotor function in SCI rats, reduced scar formation, and promoted axonal regeneration. Mechanistically, API downregulated NLRP3/ gasdermin D expression in microglia, reduced the release of inflammatory factors, and enhanced mitophagy. Notably, the protective effects of API were reversed by Mdivi-1 and mimicked by Urolithin A, confirming that mitophagy is the primary mechanism mediating API’s anti-pyroptotic effects.
Conclusion: API attenuates microglial pyroptosis and facilitates SCI repair by enhancing mitophagy-mediated clearance of damaged mitochondria and suppressing activation of the ROS/NLRP3 inflammasome pathway in rats. These findings provide important preclinical evidence supporting the development of multi-target neuroprotective strategies derived from natural compounds.
Plain Language Summary: API effectively suppresses NLRP3 inflammasome activation and mitigates microglial pyroptosis.API enhances mitophagy in microglia following SCI.API inhibits pyroptosis through mitophagy-mediated regulation of NLRP3 activation.API significantly promotes locomotor recovery and neural regeneration in spinal cord-injured rats.
Keywords: spinal cord injury, apigenin, mitophagy, pyroptosis