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已发表论文
基于中性粒细胞膜的仿生纳米平台用于脊髓损伤的靶向治疗
Authors Shang Y, Wang W, Zhang T , Qi E, Jiang R, Liu H, Wang Q, Feng S
Received 16 June 2025
Accepted for publication 7 November 2025
Published 24 November 2025 Volume 2025:20 Pages 14097—14113
DOI https://doi.org/10.2147/IJN.S547401
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Xing Zhang
Yinghui Shang,1 Wei Wang,2 Tehan Zhang,1 Enlin Qi,2 Ruizhi Jiang,2 Haiting Liu,3 Qinghai Wang,4,* Shiqing Feng1,*
1Department of Orthopaedics, the Second Qilu Hospital of Shandong University, Shandong University Centre for Orthopaedics, Shandong University, Jinan, Shandong, 250033, People’s Republic of China; 2Department of Orthopaedics, Qilu Hospital of Shandong University, Shandong University Centre for Orthopaedics, Shandong University, Jinan, Shandong, 250012, People’s Republic of China; 3Department of Blood Transfusion, Third Xiangya Hospital, Central South University, Changsha, Hunan, 410000, People’s Republic of China; 4Department of Cardiology, the Second Qilu Hospital of Shandong University, Shandong University, Jinan, Shandong, 250033, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Qinghai Wang, Department of Cardiology, the Second Qilu Hospital of Shandong University, Shandong University, Jinan, 250033, People’s Republic of China, Email sdwqh1005@126.com Shiqing Feng, Department of Orthopaedics, the Second Qilu Hospital of Shandong University, Shandong University Centre for Orthopaedics, Shandong University, Jinan, 250033, People’s Republic of China, Email shiqingfeng@sdu.edu.cn
Introduction: Spinal cord injury (SCI) triggers a cascade of secondary damage, including oxidative stress and neuroinflammation, for which effective treatments remain limited. To address this, we developed a biomimetic nanoplatform, NEU@MPBNPs-HED, consisting of mesoporous Prussian blue nanoparticles (MPBNPs) loaded with hederagenin (HED) and cloaked with neutrophil membranes (NEUm) to enhance lesion targeting and immune evasion.
Methods: The physicochemical properties, drug release characteristics, and cellular uptake of NEU@MPBNPs-HED were characterized. Therapeutic efficacy was evaluated in vitro using oxygen-glucose deprivation/reoxygenation (OGD/R) models of neuronal injury and in vivo in a murine spinal cord contusion model. Key outcomes included neuronal survival, oxidative stress, apoptosis, motor recovery, and biodistribution.
Results: In vitro, NEU@MPBNPs-HED significantly improved HT22 neuronal viability by 48.6%, reduced intracellular reactive oxygen species (ROS) by 52.4%, and preserved mitochondrial membrane potential compared with free HED or non-biomimetic controls. Apoptosis was suppressed through modulation of Bax, Bcl-2, and cytochrome C. In vivo, NEU@MPBNPs-HED enhanced Basso Mouse Scale (BMS) scores, improved motor evoked potentials, promoted axonal regeneration (NF200↑), and reduced glial scarring (GFAP↓). Moreover, the oxidative stress marker (MDA), inflammatory indicators (TNF-α, and Ly6G+ cells, and Arg1) were reduced. Biodistribution studies confirmed selective accumulation at the injury site, and histological analyses revealed no systemic toxicity.
Conclusion: The NEU@MPBNPs-HED nanoplatform effectively targeted spinal cord lesions, attenuated oxidative and inflammatory damage, and promoted neurological recovery. These findings highlight the translational potential of biomimetic nanotherapies for treating traumatic central nervous system disorders.
Keywords: spinal cord injury, neutrophil membrane, mesoporous Prussian blue nanoparticles, hederagenin, apoptosis
1Department of Orthopaedics, the Second Qilu Hospital of Shandong University, Shandong University Centre for Orthopaedics, Shandong University, Jinan, Shandong, 250033, People’s Republic of China; 2Department of Orthopaedics, Qilu Hospital of Shandong University, Shandong University Centre for Orthopaedics, Shandong University, Jinan, Shandong, 250012, People’s Republic of China; 3Department of Blood Transfusion, Third Xiangya Hospital, Central South University, Changsha, Hunan, 410000, People’s Republic of China; 4Department of Cardiology, the Second Qilu Hospital of Shandong University, Shandong University, Jinan, Shandong, 250033, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Qinghai Wang, Department of Cardiology, the Second Qilu Hospital of Shandong University, Shandong University, Jinan, 250033, People’s Republic of China, Email sdwqh1005@126.com Shiqing Feng, Department of Orthopaedics, the Second Qilu Hospital of Shandong University, Shandong University Centre for Orthopaedics, Shandong University, Jinan, 250033, People’s Republic of China, Email shiqingfeng@sdu.edu.cn
Introduction: Spinal cord injury (SCI) triggers a cascade of secondary damage, including oxidative stress and neuroinflammation, for which effective treatments remain limited. To address this, we developed a biomimetic nanoplatform, NEU@MPBNPs-HED, consisting of mesoporous Prussian blue nanoparticles (MPBNPs) loaded with hederagenin (HED) and cloaked with neutrophil membranes (NEUm) to enhance lesion targeting and immune evasion.
Methods: The physicochemical properties, drug release characteristics, and cellular uptake of NEU@MPBNPs-HED were characterized. Therapeutic efficacy was evaluated in vitro using oxygen-glucose deprivation/reoxygenation (OGD/R) models of neuronal injury and in vivo in a murine spinal cord contusion model. Key outcomes included neuronal survival, oxidative stress, apoptosis, motor recovery, and biodistribution.
Results: In vitro, NEU@MPBNPs-HED significantly improved HT22 neuronal viability by 48.6%, reduced intracellular reactive oxygen species (ROS) by 52.4%, and preserved mitochondrial membrane potential compared with free HED or non-biomimetic controls. Apoptosis was suppressed through modulation of Bax, Bcl-2, and cytochrome C. In vivo, NEU@MPBNPs-HED enhanced Basso Mouse Scale (BMS) scores, improved motor evoked potentials, promoted axonal regeneration (NF200↑), and reduced glial scarring (GFAP↓). Moreover, the oxidative stress marker (MDA), inflammatory indicators (TNF-α, and Ly6G+ cells, and Arg1) were reduced. Biodistribution studies confirmed selective accumulation at the injury site, and histological analyses revealed no systemic toxicity.
Conclusion: The NEU@MPBNPs-HED nanoplatform effectively targeted spinal cord lesions, attenuated oxidative and inflammatory damage, and promoted neurological recovery. These findings highlight the translational potential of biomimetic nanotherapies for treating traumatic central nervous system disorders.
Keywords: spinal cord injury, neutrophil membrane, mesoporous Prussian blue nanoparticles, hederagenin, apoptosis