NeuroMolecular Medicine最新文献_第2页

Exosomal GDNF from Bone Marrow Mesenchymal Stem Cells Moderates Neuropathic Pain in a Rat Model of Chronic Constriction Injury. 骨髓间充质干细胞外泌 GDNF 可缓和大鼠慢性收缩性损伤模型中的神经性疼痛

IF 3.3 4区医学

NeuroMolecular Medicine Pub Date : 2024-08-21 DOI: 10.1007/s12017-024-08800-6

Xuelei Zhang, Huan Liu, Xiaolei Xiu, Jibo Cheng, Tong Li, Ping Wang, Lili Men, Junru Qiu, Yanyan Jin, Jianyong Zhao

{"title":"Exosomal GDNF from Bone Marrow Mesenchymal Stem Cells Moderates Neuropathic Pain in a Rat Model of Chronic Constriction Injury.","authors":"Xuelei Zhang, Huan Liu, Xiaolei Xiu, Jibo Cheng, Tong Li, Ping Wang, Lili Men, Junru Qiu, Yanyan Jin, Jianyong Zhao","doi":"10.1007/s12017-024-08800-6","DOIUrl":"10.1007/s12017-024-08800-6","url":null,"abstract":"Both of exosomes derived from mesenchymal stem cells (MSCs) and glial cell line-derived neurotrophic factor (GDNF) show potential for the treatment of neuropathic pain. Here, the analgesic effects of exosomes derived from bone marrow MSCs (BMSCs) were investigated. BMSCs-derived exosomes were isolated and characterized. Chronic constriction injury (CCI) was constructed to induce neuropathic pain in rats, which were then treated with exosomes. Pain behaviors were evaluated by measuring paw withdrawal thresholds and latency. The changes of key proteins, including cytokines, were explored using Western blot and ELISA. Administration of BMSCs-derived exosomes alleviated neuropathic pain, as demonstrated by the decrease of thermal hyperalgesia and mechanical allodynia, as well as the reduced secretion of pro-inflammatory cytokines in CCI rats. These effects were comparable to the treatment of GDNF alone. Mechanically, the exosomes suppressed the CCI-induced activation of TLR2/MyD88/NF-κB signaling pathway, while GDNF knockdown impaired their analgesic effects on CCI rat. BMSCs-derived exosomes may alleviate CCI-induced neuropathic pain and inflammation in rats by transporting GDNF.","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142018169","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Activation of GPR30 Ameliorates Cerebral Ischemia-Reperfusion Injury by Suppressing Ferroptosis Through Nrf2/GPX4 Signaling Pathway. 激活 GPR30 可通过 Nrf2/GPX4 信号通路抑制铁凋亡，从而改善脑缺血再灌注损伤

IF 3.3 4区医学

NeuroMolecular Medicine Pub Date : 2024-08-13 DOI: 10.1007/s12017-024-08801-5

Yong-Qiang Zhang, Ting Sun, Zhen Zhao, Jing Fu, Le Yang, Yuan Xu, Jing-Feng Zhao, Xiu-Ling Tang, An Liu, Ming-Gao Zhao

{"title":"Activation of GPR30 Ameliorates Cerebral Ischemia-Reperfusion Injury by Suppressing Ferroptosis Through Nrf2/GPX4 Signaling Pathway.","authors":"Yong-Qiang Zhang, Ting Sun, Zhen Zhao, Jing Fu, Le Yang, Yuan Xu, Jing-Feng Zhao, Xiu-Ling Tang, An Liu, Ming-Gao Zhao","doi":"10.1007/s12017-024-08801-5","DOIUrl":"10.1007/s12017-024-08801-5","url":null,"abstract":"The newly identified estrogen receptor, G protein-coupled receptor 30 (GPR30), is prevalent in the brain and has been shown to provide significant neuroprotection. Recent studies have linked ferroptosis, a newly characterized form of programmed cell death, closely with cerebral ischemia-reperfusion injury (CIRI), highlighting it as a major contributing factor. Consequently, our research aimed to explore the potential of GPR30 targeting in controlling neuronal ferroptosis and lessening CIRI impacts. Results indicated that GPR30 activation not only improved neurological outcomes and decreased infarct size in a mouse model but also lessened iron accumulation and malondialdehyde formation post-middle cerebral artery occlusion (MCAO). This protective effect extended to increased levels of Nrf2 and GPX4 proteins. Similar protective results were replicated in PC12 cells subjected to Oxygen Glucose Deprivation and Reoxygenation (OGD/R) using the GPR30-specific agonist G1. Importantly, inhibition of Nrf2 with ML385 curtailed the neuroprotective effects of GPR30 activation, suggesting that GPR30 mitigates CIRI primarily through inhibition of neuronal ferroptosis via upregulation of Nrf2 and GPX4.","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141976253","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Evaluation of Neuroprotective Effect of Gut Microbe in Parkinson's Disease: An In Silico and In Vivo Approach. 评估肠道微生物对帕金森病的神经保护作用：体内和体外方法。

IF 3.3 4区医学

NeuroMolecular Medicine Pub Date : 2024-08-01 DOI: 10.1007/s12017-024-08799-w

Kanika Bhardwaj, Neelu Kanwar Rajawat, Nupur Mathur, Aviral Kaushik

{"title":"Evaluation of Neuroprotective Effect of Gut Microbe in Parkinson's Disease: An In Silico and In Vivo Approach.","authors":"Kanika Bhardwaj, Neelu Kanwar Rajawat, Nupur Mathur, Aviral Kaushik","doi":"10.1007/s12017-024-08799-w","DOIUrl":"https://doi.org/10.1007/s12017-024-08799-w","url":null,"abstract":"Parkinson's disease is a progressive neurodegenerative disorder marked by the death of dopaminergic neurons in the substantia nigra region of the brain. Aggregation of alpha-synuclein (α-synuclein) is a contributing factor to Parkinson's disease pathogenesis. The objective of this study is to investigate the neuroprotective effects of gut microbes on α-synuclein aggregation using both in silico and in vivo approaches. We focussed on the interaction between α-synuclein and metabolites released by gut bacteria that protect from PD. We employed three probiotic microbe strains against α-synuclein protein: Lactobacillus casei, Escherichia coli, and Bacillus subtilis, with their chosen PDB IDs being Dihydrofolate reductase (3DFR), methionine synthetase (6BM5), and tryptophanyl-tRNA synthetase (3PRH), respectively. Using HEX Dock 6.0 software, we examined the interactions between these proteins. Among the various metabolites, methionine synthetase produced by E. coli showed potential interactions with α-synuclein. To further evaluate the neuroprotective benefits of E. coli, an in vivo investigation was performed using a rotenone-induced Parkinsonian mouse model. The motor function of the animals was assessed through behavioural tests, and oxidative stress and neurotransmitter levels were also examined. The results demonstrated that, compared to the rotenone-induced PD mouse model, the rate of neurodegeneration was considerably reduced in mice treated with E. coli. Additionally, histopathological studies provided evidence of the neuroprotective effects of E. coli. In conclusion, this study lays the groundwork for future research, suggesting that gut bacteria may serve as potential therapeutic agents in the development of medications to treat Parkinson's disease. fig. 1.","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141875518","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Physical Exercise Inhibits Cognitive Impairment and Memory Loss in Aged Mice, and Enhances Pre- and Post-Synaptic Proteins in the Hippocampus of Young and Aged Mice. 体育锻炼可抑制老年小鼠的认知障碍和记忆丧失，并增强年轻小鼠和老年小鼠海马突触前后蛋白的功能

IF 3.3 4区医学

NeuroMolecular Medicine Pub Date : 2024-07-29 DOI: 10.1007/s12017-024-08798-x

Ricardo Augusto Leoni De Sousa, Caique Olegário Diniz-Magalhaes, Poliany Pereira Cruz, Gustavo Henrique Bahia de Oliveira, Julia Tereza Aparecida Caldeira Prates, Crisley Mara de Azevedo Ferreira, Rosiane Rosa Silva, Ricardo Cardoso Cassilhas

{"title":"Physical Exercise Inhibits Cognitive Impairment and Memory Loss in Aged Mice, and Enhances Pre- and Post-Synaptic Proteins in the Hippocampus of Young and Aged Mice.","authors":"Ricardo Augusto Leoni De Sousa, Caique Olegário Diniz-Magalhaes, Poliany Pereira Cruz, Gustavo Henrique Bahia de Oliveira, Julia Tereza Aparecida Caldeira Prates, Crisley Mara de Azevedo Ferreira, Rosiane Rosa Silva, Ricardo Cardoso Cassilhas","doi":"10.1007/s12017-024-08798-x","DOIUrl":"https://doi.org/10.1007/s12017-024-08798-x","url":null,"abstract":"The aim of this study was to evaluate the effects of swimming in the brain and behavior of young and aged mice. Forty-eight male C57BL/6 J mice were randomly distributed into 4 groups (n = 12 per group, 3 and 18 months old). The subdivision of the groups was: 3 months-SED, 18 months-SED, 3 months-EXE, and 18 months-EXE. SED mice did not swim, while EXE mice performed the physical exercise protocol. Training was initiated 48 h after the adaptation week. Swimming sessions consisted of 30 min, with no overload, 5 days per week, for 4 weeks. After the exercise protocol, it was revealed working and spatial memory were impaired in the 18 months-SED group. Pre- and post-synaptic proteins were enhanced in the groups that swam when compared to the 3- and 8 months-SED groups. Lipid peroxidation was greater in the aged mice that did not perform the physical exercise protocol and might have contributed to the cognitive impairment in this group. In conclusion, an aerobic physical exercise protocol, performed through regular swimming sessions, inhibited cognitive impairment, memory loss and lipid peroxidation in the aged mice, while pre- and post-synaptic proteins were enhanced in the hippocampus of young and aged mice.","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141788752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The CD44s Isoform is a Potential Biomarker for Predicting Craniopharyngioma Recurrence in Children. CD44s异构体是预测儿童颅咽管瘤复发的潜在生物标记物

IF 3.3 4区医学

NeuroMolecular Medicine Pub Date : 2024-07-17 DOI: 10.1007/s12017-024-08797-y

K Bajdak-Rusinek, N Diak, E Gutmajster, A Fus-Kujawa, M Ciupińska, B Kalina-Faska, A Trybus, M Grajek, M Kalina, M Mandera

{"title":"The CD44s Isoform is a Potential Biomarker for Predicting Craniopharyngioma Recurrence in Children.","authors":"K Bajdak-Rusinek, N Diak, E Gutmajster, A Fus-Kujawa, M Ciupińska, B Kalina-Faska, A Trybus, M Grajek, M Kalina, M Mandera","doi":"10.1007/s12017-024-08797-y","DOIUrl":"10.1007/s12017-024-08797-y","url":null,"abstract":"Adamantinomatous craniopharyngioma (ACP) is an intracranial tumor considered partly malignant due to its ability to infiltrate surrounding structures and tendency to relapse despite radical resection. CD44 is a known stem cell marker in ACP and is upregulated in cell clusters of invasive ACP protrusions; however, the functions of its alternative splicing isoform variants, CD44s and CD44v1-10, have not yet been studied in terms of ACP recurrence, despite their confirmed roles in cancer development and progression. In this study, we first confirmed the difference in total CD44 expression between samples from patients who experienced relapse and those from patients who did not. Moreover, our findings showed that, in recurrent samples, the predominant isoform expressed was CD44s, which might indicate its significance in predicting ACP recurrence. The association between increased CD44 expression and recurrence may lead to the development of prognostic markers of ACP aggressiveness and relapse potential; however, further studies are needed to clarify the exact mechanism of CD44 expression.","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11254967/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141634111","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Astaxanthin Rescues Memory Impairments in Rats with Vascular Dementia by Protecting Against Neuronal Death in the Hippocampus. 虾青素通过防止海马区神经元死亡修复血管性痴呆大鼠的记忆损伤

IF 3.3 4区医学

NeuroMolecular Medicine Pub Date : 2024-07-16 DOI: 10.1007/s12017-024-08796-z

Na Wei, Luo-Man Zhang, Jing-Jing Xu, Sheng-Lei Li, Rui Xue, Sheng-Li Ma, Cai Li, Miao-Miao Sun, Kui-Sheng Chen

{"title":"Astaxanthin Rescues Memory Impairments in Rats with Vascular Dementia by Protecting Against Neuronal Death in the Hippocampus.","authors":"Na Wei, Luo-Man Zhang, Jing-Jing Xu, Sheng-Lei Li, Rui Xue, Sheng-Li Ma, Cai Li, Miao-Miao Sun, Kui-Sheng Chen","doi":"10.1007/s12017-024-08796-z","DOIUrl":"https://doi.org/10.1007/s12017-024-08796-z","url":null,"abstract":"Vascular dementia (VaD) is a cognitive disorder characterized by a decline in cognitive function resulting from cerebrovascular disease. The hippocampus is particularly susceptible to ischemic insults, leading to memory deficits in VaD. Astaxanthin (AST) has shown potential therapeutic effects in neurodegenerative diseases. However, the mechanisms underlying its protective effects in VaD and against hippocampal neuronal death remain unclear. In this study, We used the bilateral common carotid artery occlusion (BCCAO) method to establish a chronic cerebral hypoperfusion (CCH) rat model of VaD and administered a gastric infusion of AST at 25 mg/kg per day for 4 weeks to explore its therapeutic effects. Memory impairments were assessed using Y-maze and Morris water maze tests. We also performed biochemical analyses to evaluate levels of hippocampal neuronal death and apoptosis-related proteins, as well as the impact of astaxanthin on the PI3K/Akt/mTOR pathway and oxidative stress. Our results demonstrated that AST significantly rescued memory impairments in VaD rats. Furthermore, astaxanthin treatment protected against hippocampal neuronal death and attenuated apoptosis. We also observed that AST modulated the PI3K/Akt/mTOR pathway, suggesting its involvement in promoting neuronal survival and synaptic plasticity. Additionally, AST exhibited antioxidant properties, mitigating oxidative stress in the hippocampus. These findings provide valuable insights into the potential therapeutic effects of AST in VaD. By elucidating the mechanisms underlying the actions of AST, this study highlights the importance of protecting hippocampal neurons and suggests potential targets for intervention in VaD. There are still some unanswered questions include long-term effects and optimal dosage of the use in human. Further research is warranted to fully understand the therapeutic potential of AST and its application in the clinical treatment of VaD.","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141627174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A Comprehensive Overview of NF1 Mutations in Iranian Patients. 伊朗患者 NF1 基因突变综述

IF 3.3 4区医学

NeuroMolecular Medicine Pub Date : 2024-07-02 DOI: 10.1007/s12017-024-08790-5

Shahram Savad, Mohammad-Hossein Modarressi, Sarang Younesi, Mahnaz Seifi-Alan, Niusha Samadaian, Mona Masoomy, Mehdi Dianatpour, Shima Norouzi, Saloomeh Amidi, Amirreza Boroumand, Mahmoud Reza Ashrafi, Alireza Ronagh, Maryam Eslami, Maryam Hashemnejad, Shahab Nourian, Sanaz Mohammadi, Mohammad Mahdi Taheri Amin, Morteza Heidari, Mahin Seifi-Alan, Hossein Shojaaldini Ardakani, Fatemeh Aghamahdi, Sheyda Khalilian, Soudeh Ghafouri-Fard

{"title":"A Comprehensive Overview of NF1 Mutations in Iranian Patients.","authors":"Shahram Savad, Mohammad-Hossein Modarressi, Sarang Younesi, Mahnaz Seifi-Alan, Niusha Samadaian, Mona Masoomy, Mehdi Dianatpour, Shima Norouzi, Saloomeh Amidi, Amirreza Boroumand, Mahmoud Reza Ashrafi, Alireza Ronagh, Maryam Eslami, Maryam Hashemnejad, Shahab Nourian, Sanaz Mohammadi, Mohammad Mahdi Taheri Amin, Morteza Heidari, Mahin Seifi-Alan, Hossein Shojaaldini Ardakani, Fatemeh Aghamahdi, Sheyda Khalilian, Soudeh Ghafouri-Fard","doi":"10.1007/s12017-024-08790-5","DOIUrl":"10.1007/s12017-024-08790-5","url":null,"abstract":"Neurofibromatosis type 1 (NF1) is a genetic disorder caused by mutations in the NF1 gene. This disorder shows nearly complete penetrance and high phenotypic variability. We used the whole-exome sequencing technique to identify mutations in 32 NF1 cases from 22 Iranian families. A total of 31 variants, including 30 point mutations and one large deletion, were detected. In eight cases, variants were inherited, while they were sporadic in the remaining. Seven novel variants, including c.5576 T > G, c.6658_6659insC, c.2322dupT, c.92_93insAA, c.4360C > T, c.3814C > T, and c.4565_4566delinsC, were identified. The current study is the largest in terms of the sample size of Iranian NF1 cases with identified mutations. The results can broaden the spectrum of NF1 mutations and facilitate the process of genetic counseling in the affected families.","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141492853","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Association of NID2 SNPs with Glioma Risk and Prognosis in the Chinese Population. 中国人群中 NID2 SNPs 与胶质瘤风险和预后的关系

IF 3.3 4区医学

NeuroMolecular Medicine Pub Date : 2024-06-27 DOI: 10.1007/s12017-024-08795-0

Jie Hao, Congmei Huang, Weiwei Zhao, Lin Zhao, Xiuxia Hu, WenJie Zhang, Le Guo, Xia Dou, Tianbo Jin, Mingjun Hu

{"title":"Association of NID2 SNPs with Glioma Risk and Prognosis in the Chinese Population.","authors":"Jie Hao, Congmei Huang, Weiwei Zhao, Lin Zhao, Xiuxia Hu, WenJie Zhang, Le Guo, Xia Dou, Tianbo Jin, Mingjun Hu","doi":"10.1007/s12017-024-08795-0","DOIUrl":"10.1007/s12017-024-08795-0","url":null,"abstract":"Glioma is the most common primary intracranial tumor with high mortality and poor prognosis. The purpose of this study was to investigate how single-nucleotide polymorphisms (SNPs) of the NID2 gene affect glioma risk and prognosis. Four candidate SNPs of NID2 in 529 glioma patients and 478 healthy controls were successfully genotyped by Agena MassARRAY mass spectrometer. Logistic regression was utilized to assess the associations between NID2 SNPs and glioma risk under different genetic models. Furthermore, the relationship between risk-related SNPs in NID2 and the prognosis of glioma patients was explored through Kaplan-Meier (KM) survival curve and Cox proportional hazard regression analysis. The results showed that rs11846847 (OR 1.24, p = 0.017) and rs1874569 (OR 1.22, p = 0.026) were significantly associated with an increased risk of glioma, and rs11846847 also had a risk-increasing effect on glioma in participants ≤ 40 years old. The interaction model of rs11846847 and rs1874569 could be more suitable for forecasting glioma risk. We also discovered a significant association between rs1874569 and poor prognosis in glioma patients (HR 1.32, p = 0.039) and especially CC genotype was relevant to shorter overall survival (OS) and progression-free survival (PFS) in patients with high-grade glioma. Additionally, the study demonstrated that gross total resection or chemotherapy improve glioma prognosis in the Chinese Han population. This study is the first to provide evidence for the association of NID2 SNPs with glioma risk and prognosis, suggesting that NID2 variants might be potential factors for glioma.","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141458346","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Hydrogen Sulfide can Scavenge Free Radicals to Improve Spinal Cord Injury by Inhibiting the p38MAPK/mTOR/NF-κB Signaling Pathway. 硫化氢可清除自由基，通过抑制 p38MAPK/mTOR/NF-κB 信号通路改善脊髓损伤。

IF 3.3 4区医学

NeuroMolecular Medicine Pub Date : 2024-06-21 DOI: 10.1007/s12017-024-08794-1

Kexin Lin, Yong Zhang, Yanyang Shen, Yiqin Xu, Min Huang, Xuehong Liu

引用次数: 0

Endothelial Progenitor Cells: A Review of Molecular Mechanisms in the Pathogenesis and Endovascular Treatment of Intracranial Aneurysms 内皮祖细胞：颅内动脉瘤发病机制和血管内治疗的分子机制综述

IF 3.5 4区医学

NeuroMolecular Medicine Pub Date : 2024-06-17 DOI: 10.1007/s12017-024-08791-4

Felipe Ramirez-Velandia, Emmanuel Mensah, Mira Salih, Aryan Wadhwa, Michael Young, Sandeep Muram, Philipp Taussky, Christopher S Ogilvy

引用次数: 0