Neuropeptides最新文献

{"title":"Measurement of neuropeptide Y with molecularly imprinted polypyrrole on carbon fiber microelectrodes","authors":"Luis López ,&nbsp;Kelly Lozano ,&nbsp;John Cruz ,&nbsp;Krystal Flores ,&nbsp;Lauren Fernández-Vega ,&nbsp;Lisandro Cunci","doi":"10.1016/j.npep.2024.102413","DOIUrl":"https://doi.org/10.1016/j.npep.2024.102413","url":null,"abstract":"<div><p>The measurement of neuropeptides using small electrodes for high spatial resolution would provide us with localized information on the release of neuromolecules. The release of Neuropeptide Y (NPY) is related to different neurological diseases such as stress, obesity, and PTSD, among others. In this conference paper, we electrodeposited polypyrrole on carbon fiber microelectrodes in the presence of NPY to develop a molecularly imprinted polypyrrole sensitive to NPY. Optimization of the electrodeposition process resulted in the full coverage of the polymer with nucleation sites on the carbon fiber ridges, achieving completion by the seventh cycle. Electrodeposition was performed for five cycles, and using cyclic voltammetry (CV), we studied the change in the oxidation current peak for polypyrrole due to the presence of NPY. We also observed a change in capacitance due to the presence of NPY, which was studied by electrochemical impedance spectroscopy (EIS). A linear correlation was found between the oxidation peak and the concentration of NPY between 50 ng/mL and 1000 ng/mL. In addition, a linear correlation was also found between microelectrode capacitance and the concentration of NPY between 50 ng/mL and 1000 ng/mL at 100 kHz.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"104 ","pages":"Article 102413"},"PeriodicalIF":2.9,"publicationDate":"2024-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139710131","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of NPY signaling pathway in diagnosis, prognosis and treatment of stroke","authors":"Taotao Jiang ,&nbsp;Ting Zheng ,&nbsp;Rundong Li ,&nbsp;Jingjing Sun ,&nbsp;Xiaoqing Luan ,&nbsp;Manxia Wang","doi":"10.1016/j.npep.2024.102412","DOIUrl":"10.1016/j.npep.2024.102412","url":null,"abstract":"<div><p>Neuropeptide Y (NPY), an extensively distributed neurotransmitter within the central nervous system (CNS), was initially detected and isolated from the brain of a pig in 1982. By binding to its G protein-coupled receptors, NPY regulates immune responses and contributes to the pathogenesis of numerous inflammatory diseases. The hippocampus contained the maximum concentration in the CNS, with the cerebral cortex, hypothalamus, thalamus, brainstem, and cerebellum following suit. This arrangement suggests that the substance has a specific function within the CNS. More and more studies have shown that NPY is involved in the physiological and pathological mechanism of stroke, and its serum concentration can be one of the specific biomarkers of stroke and related complications because of its high activity, broad and complex effects. By summarizing relevant literature, this article aims to gain a thorough understanding of the potential clinical applications of NPY in the treatment of stroke, identification of stroke and its related complications, and assessment of prognosis.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"104 ","pages":"Article 102412"},"PeriodicalIF":2.9,"publicationDate":"2024-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139678945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Localization of truncated TrkB and co-expression with full-length TrkB in the cerebral cortex of adult mice","authors":"Koji Ohira","doi":"10.1016/j.npep.2024.102411","DOIUrl":"10.1016/j.npep.2024.102411","url":null,"abstract":"<div><p>Brain-derived neurotrophic factor (BDNF), one of the neurotrophins, and its specific receptor TrkB, are abundantly distributed in the central nervous system (CNS) and have a variety of biological effects, such as neural survival, neurite elongation, neural differentiation, and enhancing synaptic functions. Currently, there are two TrkB subtypes: full-length TrkB (TrkB-FL), which has a tyrosine kinase in the intracellular domain, and TrkB-T1, which is a tyrosine kinase-deficient form. While TrkB-FL is a typical tyrosine kinase receptor, TrkB-T1 is a main form expressed in the CNS of adult mammals, but its function is unknown. In this study, we performed fluorescent staining of the cerebral cortex of adult mice, by using TrkB-T1 antiserum and various antibodies of marker molecules for neurons and glial cells. We found that TrkB-T1 was expressed not only in neurons but also in astrocytes. In contrast, little expression of TrkB-T1 was found in oligodendrocytes and microglia. TrkB-T1 was expressed in almost all of the cells expressing TrkB-FL, indicating the direct interaction between TrkB subtypes. These findings suggest that a part of various functions of BDNF-TrkB signaling might be due to the interaction and cellular localization of TrkB subtypes in the cerebral cortex.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"104 ","pages":"Article 102411"},"PeriodicalIF":2.9,"publicationDate":"2024-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139578964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A comparative study on the effects of human serum albumin and α-melanocyte-stimulating hormone fusion proteins on the anti-neuroinflammatory in the central nervous system of adult mice","authors":"Yiyao Liu ,&nbsp;Yang Li ,&nbsp;Xueyan Wei ,&nbsp;Inam Ullah ,&nbsp;Shahab Uddin ,&nbsp;Jiatao Wang ,&nbsp;Runjie Xia ,&nbsp;Meizhu Wang ,&nbsp;Hui Yang ,&nbsp;Hongyu Li","doi":"10.1016/j.npep.2024.102410","DOIUrl":"10.1016/j.npep.2024.102410","url":null,"abstract":"<div><p><span>The immunomodulatory effects of α-melanocyte stimulating hormone (α-MSH) in the central nervous system<span> (CNS) have been investigated for forty years. The clinical applications of α-MSH are limited due to its short half-life. Our previous study has indicated that the short half-life of α-MSH can be extended by fusion with carrier human serum albumin<span> (HSA) and this fusion protein has also retained the anti-inflammatory effect on the CNS. This improvement is still far from the clinical requirements. Thus, we expected to enhance the half-life and activity of the fusion protein by optimizing the linker peptide to get closer to clinical requirements. In a previous study, we screened out two candidates </span></span></span><em>in vitro</em> experiments with a flexible linker peptide (fusion protein with flexible linker peptide, FPFL) and a rigid linker peptide (fusion protein with rigid linker peptide, FPRL), respectively. However, it was not sure whether the anti-inflammatory effects <em>in vitro</em> could be reproduced <em>in vivo</em>. Our results show that FPRL is the best candidate with a longer half-life compared to the traditional flexible linker peptides. Meanwhile, the ability of FPRL to penetrate the blood-brain barrier (BBB) was enhanced, and the inhibition of TNF-α and IL-6 was improved. We also found that the toxicity of FPRL was decreased. All of the results suggested that trying to choose the rigid linker peptide in some fusion proteins may be a potential choice for improving the unsatisfactory characteristics.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"104 ","pages":"Article 102410"},"PeriodicalIF":2.9,"publicationDate":"2024-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139551794","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cyclooxygenase-2 inhibition affects the ratio of GluN2A/GluN2B receptor subunits through interaction with mGluR5 in the mouse brain","authors":"Katarzyna Stachowicz ,&nbsp;Patrycja Pańczyszyn-Trzewik ,&nbsp;Paulina Misztak ,&nbsp;Szymon Rzeźniczek ,&nbsp;Magdalena Sowa-Kućma","doi":"10.1016/j.npep.2024.102409","DOIUrl":"10.1016/j.npep.2024.102409","url":null,"abstract":"<div><p><em>N</em><span><span>-methyl-D-aspartic acid receptors (NMDARs) are the most studied receptors in mammalian brains. Their role in depression, cognition, schizophrenia<span>, learning and memorization, Alzheimer's disease, and more is well documented. In the search for new </span></span>drug<span><span><span> candidates in depression, intensive studies have been conducted. Compounds that act by influencing NMDARs have been particularly intensively investigated following the success of ketamine<span> in clinics. Unfortunately, the side effects associated with ketamine do not allow it to be useful in all cases. Therefore, it is important to learn about new unknown mechanisms related to NMDAR activation and study the impact of changes in the excitatory synapse environment on this receptor. Both direct and intermediary influence on NMDARs via mGluRs and COX-2 are effective. Our prior studies showed that both mGluRs ligands and COX-2 inhibitors are potent in depression-like and cognitive studies through mutual interactions. The side effects associated with </span></span>imipramine<span> administration, e.g., memory impairment, were improved when inhibiting COX-2. Therefore, this study is a trial that involves searching for modifications in NMDARs in mouse brains after prolonged treatment with </span></span>MTEP<span> (mGluR5 antagonist), NS398<span><span> (COX-2 inhibitor), or imipramine (tricyclic antidepressant). The prefrontal cortex<span> (PFC) and hippocampus (HC) were selected for PCR and </span></span>Western blot analyses. Altered expression of </span></span></span></span><em>Gin2a</em> or <em>Grin2b</em> genes after treatment was found. The observed effects were more potent when COX-2 was inhibited. The finding described here may be vital when searching for new drugs acting via NMDARs without the side effects related to cognition.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"104 ","pages":"Article 102409"},"PeriodicalIF":2.9,"publicationDate":"2024-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139500620","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunohistochemical determination of the excitatory and inhibitory axonal endings contacting NUCB2/nesfatin-1 neurons","authors":"Aynura Aghayeva,&nbsp;Duygu Gok Yurtseven,&nbsp;Nursel Hasanoglu Akbulut,&nbsp;Ozhan Eyigor","doi":"10.1016/j.npep.2023.102401","DOIUrl":"10.1016/j.npep.2023.102401","url":null,"abstract":"<div><p>Nesfatin-1 is an anorexigenic peptide suppressing food intake and is synthesized and secreted by neurons located in the hypothalamus. Our study was aimed to demonstrate the effect of excitatory and inhibitory neurotransmitters on NUCB2/nesfatin-1 neurons. In this context, dual peroxidase immunohistochemistry staining was performed using NUCB2/nesfatin-1 primary antibody with each of the primary antibodies of vesicular transporter proteins applied as markers for neurons using glutamate, acetylcholine, and GABA as neurotransmitters. In double labeling applied on floating sections, the NUCB2/nesfatin-1 reaction was determined in brown color with diaminobenzidine, while vesicular carrier proteins were marked in black. Slides were analyzed to determine the ratio of nesfatin-1 neurons in the three hypothalamic nucleus in contact with a relevant vesicular carrier protein. The ratios of NUCB2/nesfatin-1 neurons with the innervation were compared among neurotransmitters. In addition, possible gender differences between males and females were examined. The difference in the number of VGLUT2-contacting NUCB2/nesfatin-1 neurons was significantly higher in males when compared to females. When both genders were compared in different nuclei, it was seen that there was no statistical significance in terms of the percentage of NUCB2/nesfatin-1 neuron apposition with VGLUT3. The statistical evaluation showed that number of NUCB2/nesfatin-1 neurons receiving GABAergic innervation is higher in males when compared to females (*<em>p</em> ≤ 0.05; <em>p</em> = 0.045). When the axonal contact of vesicular neurotransmitter transporter proteins was compared between the neurotransmitters, it was determined that the most prominent innervation is GABAergic. In the supraoptic region, no contacts of VAChT-containing axons were found on NUCB2/nesfatin-1 neurons in both female and male subjects. In conclusion, it is understood that both excitatory and inhibitory neurons can innervate the NUCB2/nesfatin-1 neurons and the glutamatergic system is effective in the excitatory innervation while the GABAergic system plays a role in the inhibitory mechanism.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"103 ","pages":"Article 102401"},"PeriodicalIF":2.9,"publicationDate":"2023-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0143417923000823/pdfft?md5=176b747a2df34b78779d0777d53f9d32&pid=1-s2.0-S0143417923000823-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139035428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CircBUB1 activates the PI3K/AKT signaling pathway to promote the migration and invasion of glioblastoma cells","authors":"Runan Zhang, Dongmei Wu, Ying Wang, Liping Wu, Guowei Gao, Dayong Shan","doi":"10.1016/j.npep.2023.102400","DOIUrl":"https://doi.org/10.1016/j.npep.2023.102400","url":null,"abstract":"<h3>Background</h3><p>Glioblastoma (GBM) is the most aggressive primary brain tumor, characterized by rapid growth and resistance to treatment, leading to poor survival rates. The molecular mechanisms underlying GBM progression remain unclear, necessitating further research. This study focuses on the role of circBUB1, a circular RNA, in GBM cell migration and invasion, and the associated molecular mechanisms.</p><h3>Methods</h3><p>RNA/protein expression was detected using RT-qPCR/western blot assay. Transwell and wound healing assays were conducted to assess GBM cell migration and invasion. Detailed mechanistic analyses were carried out to understand the role of circBUB1 in GBM cells.</p><h3>Results</h3><p>CircBUB1 was found to be highly expressed and functioned as an oncogene in GBM cells. Functional assays revealed that knockdown of circBUB1 suppressed the migration and invasion of GBM cells. Mechanistic analyses showed that circBUB1 sequestered miR-1296-5p, thereby elevating TRIM14 expression. TRIM14 was also found to promote PTEN ubiquitination, ultimately leading to the down-regulation of PTEN protein and activation of the PI3K/AKT signaling pathway. Through rescue assays, this study confirmed that circBUB1 promoted GBM cell migration and invasion by reducing PTEN protein levels.</p><h3>Conclusion</h3><p>Our findings indicate that circBUB1 activates the PI3K/AKT signaling pathway, promoting the migration and invasion of GBM cells via the miR-1296-5p/TRIM14 axis. This provides new insights into the molecular mechanisms of GBM progression and potential therapeutic targets.</p>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"19 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138690805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of somatostatin, a somatostatin agonist, and an antagonist, on a putative migraine trigger pathway","authors":"Geoffrey A. Lambert ,&nbsp;Alessandro S. Zagami","doi":"10.1016/j.npep.2023.102399","DOIUrl":"10.1016/j.npep.2023.102399","url":null,"abstract":"<div><h3>Objective</h3><p>To determine whether somatostatin (SST) could be a cortico-brainstem neurotransmitter involved in producing the headache of migraine.</p></div><div><h3>Background</h3><p>There is evidence to support the idea that a cortico-brainstem-trigeminal nucleus neuraxis might be responsible for producing migraine headache; we have suggested that SST may be one of the neurotransmitters involved.</p></div><div><h3>Methods</h3><p>Rats were anesthetised and prepared for recording neurons in either the periaqueductal gray matter (PAG) or nucleus raphe magnus (NRM), as well as the trigeminal nucleus caudalis (TNC). The dura mater and facial skin were stimulated electrically or mechanically. SST, the SST agonist L054264 and the SST antagonist CYN54806 were injected intravenously, by microinjection, or by iontophoresis into the PAG or NRM. Cortical neuronal activity was provoked by cortical spreading depression (CSD) or light flash (LF) and was monitored by recording cortical blood flow (CBF).</p></div><div><h3>Results</h3><p>Intravenous injection of SST: (a) selectively decreased the responses of TNC neurons to stimulation of the dura, but not skin, for up to 5 h; (b) decreased the ongoing discharge rate of TNC neurons while simultaneously increasing the discharge rate of neurons in either brainstem nucleus and; (c) prevented, or reversed, the effect of CSD and LF on brainstem and trigeminal neuron discharge rates. CSD and LF decreased the discharge rate of neurons in both brainstem nuclei and increased the discharge rate of TNC neurons. These effects were reversed by L054264 and mimicked by CYN54806. Injections of L054264 into the PAG or NRM reduced the response of TNC neurons to dural stimulation and skin stimulation differentially, depending on the nucleus injected. Injections of CYN54806 into either brainstem nucleus potentiated the responses of TNC neurons to dural and skin stimulation, but without a marked differential effect.</p></div><div><h3>Conclusions</h3><p>These results imply that SST could be a neurotransmitter in a pathway responsible for migraine pain.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"103 ","pages":"Article 102399"},"PeriodicalIF":2.9,"publicationDate":"2023-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S014341792300080X/pdfft?md5=d52cfad0b3101d4f39777e5b79ba3e38&pid=1-s2.0-S014341792300080X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138579172","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"New fraternine analogues: Evaluation of the antiparkinsonian effect in the model of Parkinson's disease","authors":"Andréia Biolchi Mayer ,&nbsp;Henrique de Oliveira Amaral ,&nbsp;Danilo Gustavo R. de Oliveira ,&nbsp;Gabriel Avohay Alves Campos ,&nbsp;Priscilla Galante Ribeiro ,&nbsp;Solange Cristina Rego Fernandes ,&nbsp;Adolfo Carlos Barros de Souza ,&nbsp;Raffael Júnio Araújo de Castro ,&nbsp;Anamélia Lorenzetti Bocca ,&nbsp;Márcia Renata Mortari","doi":"10.1016/j.npep.2023.102390","DOIUrl":"10.1016/j.npep.2023.102390","url":null,"abstract":"<div><p>Venom-derived peptides are important sources for the development of new therapeutic molecules, especially due to their broad pharmacological activity. Previously, our research group identified a novel natural peptide, named fraternine, with promising effects for the treatment of Parkinson's disease. In the present paper, we synthesized three peptides bioinspired in fraternine: fra-10, fra-14, and fra-24. They were tested in the 6-OHDA-induced model of parkinsonism, quantifying motor coordination, levels of TH+ neurons in the <em>substantia nigra pars compacta</em> (SN), and inflammation mediators TNF-α, IL-6, and IL-1ß in the cortex. Peptides fra-14 and fra-10 improved the motor coordination in relation to 6-OHDA lesioned animals. However, most of the peptides were toxic in the doses applied. All three peptides reduced the intensity of the lesion induced rotations in the apomorphine test. Fra-24 higher dose increased the number of TH+ neurons in SN and reduced the concentration of TNF-α in the cortex of 6-OHDA lesioned mice. Overall, only the peptide fra-24 presented a neuroprotection effect on dopaminergic neurons of SN and a reduction of cytokine TNF-α levels, making it worthy of consideration for the treatment of PD.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"103 ","pages":"Article 102390"},"PeriodicalIF":2.9,"publicationDate":"2023-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0143417923000719/pdfft?md5=c496fa6bb627804800a78cf237e1f4da&pid=1-s2.0-S0143417923000719-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135714404","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of valproic acid combined with transplantation of olfactory ensheathing cells modified by neurotrophic 3 gene on nerve protection and repair after traumatic brain injury","authors":"Haiming Li ,&nbsp;Zhijie Yin ,&nbsp;Shuangzhu Yue ,&nbsp;Yunying An ,&nbsp;Xiaoyin Wang ,&nbsp;Shifang Zhou ,&nbsp;Lei Meng ,&nbsp;Baozhe Jin","doi":"10.1016/j.npep.2023.102389","DOIUrl":"10.1016/j.npep.2023.102389","url":null,"abstract":"<div><h3>Background</h3><p>Traumatic brain injury (TBI) often leads to cognitive and neurological dysfunction. Valproic acid (VPA) has a neuroprotective effect in acute central nervous system diseases; the neurotrophin 3 gene (NT-3) can maintain the survival of neurons, and olfactory ensheathing cells (OECs) can promote the growth of nerve axons. This study aimed to evaluate the restorative effect of VPA combined with NT-3 modified OECs (NT-3-OECs) on neurological function after TBI.</p></div><div><h3>Methods</h3><p>The neurological severity score (NSS) of rats was evaluated on the 1st, 7th, 14th, and 28th day after TBI modeling and corresponding intervention. Hematoxylin-eosin (HE) staining, p75 nerve growth factor receptor (P75), glial fibrillary acidic protein (GFAP), and neurofilament protein (NF)staining, and argyrophilic staining were used to observe the morphology of brain tissue 28 days after modeling. Moreover, TdT-mediated dUTP Nick-End Labeling (TUNEL) was used to detect the apoptosis rate of neurons. The changes in synapses and mitochondria in the injured area were observed by electron microscope.</p></div><div><h3>Results</h3><p>NT-3-OECs transplantation can increase the content of NT-3 in brain tissue, and NT-3-OECs can survive for &gt;28 days. The NSS score of the TBI-VPA-NT-3-OECs group 28 days after cell transplantation was significantly lower than that of the other model treatment groups (<em>P</em> &lt; 0.05). The morphological structure of the brain tissue was more complete, and the neurofilament fibers were neatly arranged, achieving better results than those of the other groups. The apoptosis rate of nerve cells in the TBI-VPA-NT-3-OECs group was significantly lower than in the other treatment groups (<em>P</em> &lt; 0.05). Furthermore, the number of synapses in the combined intervention group was significantly higher than in the other treatment groups, and the mitochondrial structure was more complete.</p></div><div><h3>Conclusion</h3><p>NT-3-OECs have good biological function, and VPA combined with NT-3-OECs transplantation can effectively improve the prognosis of TBI rats.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"103 ","pages":"Article 102389"},"PeriodicalIF":2.9,"publicationDate":"2023-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0143417923000707/pdfft?md5=a98bf69cb4847868e487fb1ce0a72898&pid=1-s2.0-S0143417923000707-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72014934","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}