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Polyphyllin Ⅰ enhances tumor necrosis factor-related apoptosis-inducing ligand-induced inhibition of human osteosarcoma cell growth via downregulating the Wnt/β-catenin pathway

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Journal of Traditional Chinese Medicine 2024年第2期44卷 251-259页

作者： CHANG Junli ZHAO Fulai SUN Xingyuan MA Xiaoping ZHAO Peng ZHOU Chujie SHI Binhao GU Wenchao WANG Yongjun YANG Yanping spine Disease Institute Longhua Hospital Affiliated to Shanghai University of Traditional Chinese MedicineShanghai 200032China department of Diagnostic and Interventional Radiology University of TsukubaIbaraki 315-0114Japan

OBJECTIVE:To investigate the synergistic effects of polyphyllin Ⅰ(PPⅠ)combined with tumor necrosis factorrelated apoptosis-inducing ligand(TRAIL)on the growth of osteosarcoma cells through downregulating the Wnt/β-catenin signaling pathway.METHODS:Cell viability,apoptosis and cell cycle distribution were examined using cell counting kit-8 and flow cytometry assays.The morphology of cancer cells was observed with inverted phase contrast microscope.The migration and invasion abilities were examined by xCELLigence real time cell analysis DP system and transwell assays.The expressions of poly(adenosine diphosphate-ribose)polymerase,C-Myc,Cyclin B1,cyclin-dependent kinases 1,N-cadherin,Vimentin,Active-β-catenin,β-catenin,p-glycogen synthase kinase 3β(GSK-3β)and GSK-3βwere determined by Western blotting assay.RESULTS:PPⅠ sensitized TRAIL-induced decrease of viability,migration and invasion,as well as increase of apoptosis and cell cycle arrest of MG-63 and U-2 OS osteosarcoma cells.The synergistic effect of PPⅠwith TRAIL in inhibiting the growth of osteosarcoma cells was at least partially realized through the inactivation of Wnt/β-catenin signaling pathway.CONCLUSION:The combination of PPⅠ and TRAIL is potentially a novel treatment strategy of osteosarcoma.

关键词： osteosarcoma tumor necrosis factor-related apoptosis-inducing ligand Wnt signaling pathway beta-catenin polyphyllinⅠ

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Peripheral blood RNA biomarkers can predict lesion severity in degenerative cervical myelopathy

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Neural Regeneration Research 2025年第6期 1764-1775页

作者： Zhenzhong Zheng Jialin Chen Jinghong Xu Bin Jiang Lei Li Yawei Li Yuliang Dai Bing Wang department of spine Surgery The Second Xiangya Hospital of Central South University

Degenerative cervical myelopathy is a common cause of spinal cord injury, with longer symptom duration and higher myelopathy severity indicating a worse prognosis. While numerous studies have investigated serological biomarkers for acute spinal cord injury, few studies have explored such biomarkers for diagnosing degenerative cervical myelopathy. This study involved 30 patients with degenerative cervical myelopathy（51.3 ± 7.3 years old, 12 women and 18 men）, seven healthy controls（25.7 ± 1.7 years old, one woman and six men）, and nine patients with cervical spondylotic radiculopathy（51.9 ± 8.6 years old, three women and six men）. Analysis of blood samples from the three groups showed clear differences in transcriptomic characteristics. Enrichment analysis identified 128 differentially expressed genes that were enriched in patients with neurological disabilities. Using least absolute shrinkage and selection operator analysis, we constructed a five-gene model（TBCD, TPM2, PNKD, EIF4G2, and AP5Z1） to diagnose degenerative cervical myelopathy with an accuracy of 93.5%. One-gene models（TCAP and SDHA） identified mild and severe degenerative cervical myelopathy with accuracies of 83.3% and 76.7%, respectively. Signatures of two immune cell types（memory B cells and memory-activated CD4+T cells） predicted levels of lesions in degenerative cervical myelopathy with 80% accuracy. Our results suggest that peripheral blood RNA biomarkers could be used to predict lesion severity in degenerative cervical myelopathy.

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Pharmacological interventions targeting the microcirculation following traumatic spinal cord injury

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Neural Regeneration Research 2024年第1期19卷 35-42页

作者： Rongrong Wang Jinzhu Bai department of spine and Spinal Cord Surgery Beijing Bo’ai HospitalChina Rehabilitation Research CenterBeijingChina School of Rehabilitation Medicine Capital Medical UniversityBeijingChina

Traumatic spinal cord injury is a devastating disorder chara cterized by sensory,motor,and autonomic dysfunction that seve rely compromises an individual's ability to perform activities of daily living.These adve rse outcomes are closely related to the complex mechanism of spinal cord injury,the limited regenerative capacity of central neurons,and the inhibitory environment fo rmed by traumatic injury.Disruption to the microcirculation is an important pathophysiological mechanism of spinal cord injury.A number of therapeutic agents have been shown to improve the injury environment,mitigate secondary damage,and/or promote regeneration and repair.Among them,the spinal cord microcirculation has become an important target for the treatment of spinal cord injury.Drug inte rventions targeting the microcirculation can improve the microenvironment and promote recovery following spinal cord injury.These drugs target the structure and function of the spinal cord microcirculation and are essential for maintaining the normal function of spinal neuro ns,axons,and glial cells.This review discusses the pathophysiological role of spinal cord microcirculation in spinal cord injury,including its structure and histopathological changes.Further,it summarizes the progress of drug therapies targeting the spinal cord mic rocirc ulation after spinal cord injury.

关键词： blood-spinal cord barrier drug therapy microcirculation microvascular blood flow neuroprotection pharmacological intervention pharmacotherapy spinal cord injury trauma

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Biochanin A attenuates spinal cord injury in rats during early stages by inhibiting oxidative stress and inflammasome activation

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Neural Regeneration Research 2024年第9期19卷 2050-2056页

作者： Xigong Li Jing Fu Ming Guan Haifei Shi Wenming Pan Xianfeng Lou department of Orthopedics The First Affiliated Hospital of Zhejiang UniversityHangzhouZhejiang ProvinceChina department of Stomatology Xixi HospitalHangzhouZhejiang ProvinceChina department of Orthopedics and Spine Surgerythe Affiliated Hospital of Xuzhou Medical Schoolthe Second People’s Hospital of ChangshuChangshuJiangsu ProvinceChina

Previous studies have shown that Biochanin A,a flavonoid compound with estrogenic effects,can serve as a neuroprotective agent in the context of cerebral ischemia/reperfusion injury;howeve r,its effect on spinal cord injury is still unclea r. In this study,a rat model of spinal cord injury was established using the heavy o bject impact method,and the rats were then treated with Biochanin A(40 mg/kg) via intrape ritoneal injection for 14 consecutive days.The res ults showed that Biochanin A effectively alleviated spinal cord neuronal injury and spinal co rd tissue injury,reduced inflammation and oxidative stress in spinal cord neuro ns,and reduced apoptosis and pyroptosis.In addition,Biochanin A inhibited the expression of inflammasome-related proteins(ASC,NLRP3,and GSDMD)and the Toll-like receptor 4/nuclear factor-κB pathway,activated the Nrf2/heme oxygenase 1 signaling pathway,and increased the expression of the autophagy markers LC3 Ⅱ,Beclin-1,and P62.Moreove r,the therapeutic effects of Biochanin A on early post-s pinal cord injury were similar to those of methylprednisolone.These findings suggest that Biochanin A protected neurons in the injured spinal cord through the Toll-like receptor 4/nuclear factor κB and Nrf2/heme oxygenase 1 signaling pathways.These findings suggest that Biochanin A can alleviate post-spinal cord injury at an early stage.

关键词： apoptosis autophagy Biochanin A heme oxygenase 1 inflammation Nrf2 protein nuclear factor kappa-B oxidative stress spinal cord injury Toll-like receptor 4

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Resident immune responses to spinal cord injury:role of astrocytes and microglia

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Neural Regeneration Research 2024年第8期19卷 1678-1685页

作者： Sydney Brockie Cindy Zhou Michael G.Fehlings Division of Genetics and Development Krembil Research InstituteUniversity Health NetworkTorontoONCanada Institute of Medical Science University of TorontoTorontoONCanada Division of Neurosurgery and spine Program Department of SurgeryUniversity of TorontoTorontoONCanada

Spinal cord injury can be traumatic or non-traumatic in origin,with the latter rising in incidence and prevalence with the aging demographics of our society.Moreove r,as the global population ages,individuals with co-existent degenerative spinal pathology comprise a growing number of traumatic spinal cord injury cases,especially involving the cervical spinal cord.This makes recovery and treatment approaches particula rly challenging as age and comorbidities may limit regenerative capacity.For these reasons,it is critical to better understand the complex milieu of spinal cord injury lesion pathobiology and the ensuing inflammatory response.This review discusses microglia-specific purinergic and cytokine signaling pathways,as well as microglial modulation of synaptic stability and plasticity after injury.Further,we evaluate the role of astrocytes in neurotransmission and calcium signaling,as well as their border-forming response to neural lesions.Both the inflammatory and reparative roles of these cells have eluded our complete understanding and remain key therapeutic targets due to their extensive structural and functional roles in the nervous system.Recent advances have shed light on the roles of glia in neurotransmission and reparative injury responses that will change how interventions are directed.Understanding key processes and existing knowledge gaps will allow future research to effectively target these cells and harness their regenerative potential.

关键词： astrocytes glial signaling microglia spinal cord injury synaptic transmission

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An analysis of the transcriptional landscape in hypoxia-treated primary nucleus pulposus cells

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Genes & Diseases 2024年第2期11卷 558-560页

作者： Zhicai Peng Zhuo Wang Shuaichi Guo Bing Tan Ruichao Cao Shengqiang Cheng Jun Chen Chunwang Xie Dehong Mao Zhenming Hu department of Orthopaedics Yongchuan Traditional Chinese Medicine Hospital of ChongqingChongqing 402160China department of Orthopaedic Surgery The First Affiliated Hospital of Chongqing Medical UniversityChongqing 400010China department of spine Surgery The Third Hospital of MianyangSichuan Mental Health CenterMianyangSichuan 621000China

Intervertebral disc degeneration(IDD)is the main cause of lower back pain.Lower back pain places a huge burden on society,and all current treatments for IDD cannot restore the original function of the intervertebral disc.Proposing new treatments for IDD requires clarifying the mechanisms of IDD.Physiological hypoxia is an important feature of the nucleus pulposus because of its special anatomical structure.Using RNA sequencing(RNA-seq),we obtained the whole transcriptome of nucleus pulposus cells(NPCs)under hypoxia and hypoxia-inducible factor(HIF1A)deletion.Results demonstrated possible effects of oxygen concentration and HIF1A on NPCs.In addition,our results showed that hypoxia can affect lipid metabolism in NPCs.

关键词： structure metabolism degeneration

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Lupenone improves motor dysfunction in spinal cord injury mice through inhibiting the inflammasome activation and pyroptosis in microglia via the nuclear factor kappa B pathway

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Neural Regeneration Research 2024年第8期19卷 1802-1811页

作者： Fudong Li Xiaofei Sun Kaiqiang Sun Fanqi Kong Xin Jiang Qingjie Kong department of Orthopedics Shanghai General HospitalShanghai Jiao Tong University School of MedicineShanghaiChina department of Orthopedic Surgery Spine CenterShanghai Changzheng HospitalNaval Medical UniversityShanghaiChina department of Orthopedic Surgery Naval Medical CenterNaval Medical UniversityShanghaiChina department of Anesthesiology Shanghai Changzheng HospitalNaval Medical UniversityShanghaiChina

Spinal cord injury-induced motor dysfunction is associated with neuroinflammation.Studies have shown that the triterpenoid lupenone,a natural product found in various plants,has a remarkable anti-inflammatory effect in the context of chronic inflammation.However,the effects of lupenone on acute inflammation induced by spinal cord injury remain unknown.In this study,we established an impact-induced mouse model of spinal cord injury,and then treated the injured mice with lupenone(8 mg/kg,twice a day)by intrape ritoneal injection.We also treated BV2 cells with lipopolysaccharide and adenosine5’-triphosphate to simulate the inflammatory response after spinal cord injury.Our res ults showed that lupenone reduced IKBa activation and p65 nuclear translocation,inhibited NLRP3 inflammasome function by modulating nuclear factor kappa B,and enhanced the conve rsion of proinflammatory M1 mic roglial cells into anti-inflammatory M2 microglial cells.Furthermore,lupenone decreased NLRP3 inflammasome activation,NLRP3-induced mic roglial cell polarization,and microglia pyroptosis by inhibiting the nuclear factor kappa B pathway.These findings suggest that lupenone protects against spinal cord injury by inhibiting inflammasomes.

关键词： inflammasome inflammation lupenone microglia polarization pyroptosis spinal cord injury

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Hydroxyapatite/palmitic acid superhydrophobic composite coating on AZ31 magnesium alloy with both corrosion resistance and bacterial inhibition

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Frontiers of Materials Science 2024年第1期18卷 71-83页

作者： Hang Zhang Shu Cai Huanlin Zhang Lei Ling You Zuo Hao Tian Tengfei Meng Guohua Xu Xiaogang Bao Mintao Xue Key Laboratory for Advanced Ceramics and Machining Technology of Ministry of Education Tianjin UniversityTianjin 300072China department of Orthopedic Surgery Spine CenterChangzheng HospitalNaval Medical UniversityShanghai 200003China

The coating-modified magnesium(Mg)alloys exhibit controllable corrosion resistance,but the insufficient antibacterial performance limits their clinical applications as degradable implants.Superhydrophobic coatings show excellent performance in terms of both corrosion resistance and inhibition of bacterial adhesion and growth.In this work,a hydroxyapatite(HA)/palmitic acid(PA)superhydrophobic composite coating was fabricated on the Mg alloy by the hydrothermal technique and immersion treatment.The HA/PA composite coating showed superhydrophobicity with a contact angle of 153°and a sliding angle of 2°.The coated Mg alloy exhibited excellent corrosion resistance in the simulated body fluid,with high polarization resistance(77.10 kΩ·cm^(2))and low corrosion current density((0.491±0.015)μA·cm^(-2)).Meanwhile,the antibacterial efficiency of the composite coating was over 98% against E.coli and S.aureus in different periods.The results indicate that the construction of such superhydrophobic composite coating(HA/PA)on the Mg alloy can greatly improve the corrosion resistance of Mg alloy implants within the human body and avoid bacterial infection during the initial stages of implantation.

关键词： superhydrophobic coating hydroxyapatite corrosion resistance antibacterial

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Single-cell sequencing technology in diabetic wound healing:New insights into the progenitors-based repair strategies

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World Journal of Stem Cells 2024年第5期16卷 462-466页

作者： Zhen Xiang Rui-Peng Cai Yang Xiao Yong-Can Huang Shenzhen Engineering Laboratory of Orthopaedic Regenerative Technologies Department of Spine SurgeryPeking University Shenzhen HospitalShenzhen 518036Guangdong ProvinceChina department of Breast and Thyroid Surgery Peking University Shenzhen HospitalShenzhen 518036Guangdong ProvinceChina

Diabetes mellitus(DM),an increasingly prevalent chronic metabolic disease,is characterised by prolonged hyperglycaemia,which leads to long-term health consequences.Although much effort has been put into understanding the pathogenesis of diabetic wounds,the underlying mechanisms remain unclear.The advent of single-cell RNA sequencing(scRNAseq)has revolutionised biological research by enabling the identification of novel cell types,the discovery of cellular markers,the analysis of gene expression patterns and the prediction of develop-mental trajectories.This powerful tool allows for an in-depth exploration of pathogenesis at the cellular and molecular levels.In this editorial,we focus on progenitor-based repair strategies for diabetic wound healing as revealed by scRNAseq and highlight the biological behaviour of various healing-related cells and the alteration of signalling pathways in the process of diabetic wound healing.ScRNAseq could not only deepen our understanding of the complex biology of diabetic wounds but also identify and validate new targets for inter-vention,offering hope for improved patient outcomes in the management of this challenging complication of DM.

关键词： Single-cell sequencing Diabetic wound healing Cell subpopulations Heterogeneity Pathogenesis Progenitor cells

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Argatroban promotes recovery of spinal cord injury by inhibiting the PAR1/JAK2/STAT3 signaling pathway

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Neural Regeneration Research 2024年第2期19卷 434-439页

作者： Chenxi Zhao Tiangang Zhou Ming Li Jie Liu Xiaoqing Zhao Yilin Pang Xinjie Liu Jiawei Zhang Lei Ma Wenxiang Li Xue Yao Shiqing Feng department of Orthopedics Tianjin Medical University General HospitalTianjinChina International Science and Technology Cooperation Base of Spinal Cord Injury Tianjin Key Laboratory of Spine and Spinal Cord InjuryDepartment of OrthopedicsTianjin Medical University General HospitalTianjinChina Orthopedic Research Center of Shandong University Cheeloo College of MedicineDepartment of OrthopedicsQilu Hospital of Shandong UniversityJinanShandong ProvinceChina

Argatroban is a synthetic thrombin inhibitor approved by U.S.Food and Drug Administration for the treatment of thrombosis.However,whether it plays a role in the repair of spinal cord injury is unknown.In this study,we established a rat model of T10 moderate spinal cord injury using an NYU Impactor ModerⅢand performed intraperitoneal injection of argatroban for 3 consecutive days.Our results showed that argatroban effectively promoted neurological function recovery after spinal cord injury and decreased thrombin expression and activity in the local injured spinal cord.RNA sequencing transcriptomic analysis revealed that the differentially expressed genes in the argatroban-treated group were enriched in the JAK2/STAT3 pathway,which is involved in astrogliosis and glial scar formation.Western blotting and immunofluorescence results showed that argatroban downregulated the expression of the thrombin receptor PAR1 in the injured spinal cord and the JAK2/STAT3 signal pathway.Argatroban also inhibited the activation and proliferation of astrocytes and reduced glial scar formation in the spinal cord.Taken together,these findings suggest that argatroban may inhibit astrogliosis by inhibiting the thrombin-mediated PAR1/JAK2/STAT3 signal pathway,thereby promoting the recovery of neurological function after spinal cord injury.

关键词： argatroban astrogliosis JAK/STAT signaling pathway protease-activated receptor-1 spinal cord injury thrombin vimentin

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