Current Neuropharmacology最新文献_第10页

Neurobehavioral Disorders and Cognitive Impairment in Methcathinone Exposure: A Systematic Review of Literature. 甲卡西酮暴露的神经行为障碍和认知障碍：文献系统综述。

IF 4.8 2区医学

Current Neuropharmacology Pub Date : 2025-03-25 DOI: 10.2174/011570159X387589250318041633

Yihan Wang, Ning Wang, Shuquan Zhao

{"title":"Neurobehavioral Disorders and Cognitive Impairment in Methcathinone Exposure: A Systematic Review of Literature.","authors":"Yihan Wang, Ning Wang, Shuquan Zhao","doi":"10.2174/011570159X387589250318041633","DOIUrl":"https://doi.org/10.2174/011570159X387589250318041633","url":null,"abstract":"Background: Methcathinone, a synthetic cathinone derivative similar to amphetamine, has transitioned from a 1920s ephedrine precursor and Soviet-era antidepressant to a recreationally used substance since the 1970s-1980s, raising public health concerns due to its addiction potential and neurotoxicity-related health risks.Objective: This review comprehensively analyzes methcathinone's impact on adult offspring, synthesizing recent advancements and critiquing literature to pinpoint key findings, challenges, and future research directions.Method: The systematic review adhered to PRISMA guidelines and encompassed case series, prospective and retrospective studies, as well as short communications published in English. An electronic search was conducted on PubMed, Elsevier, and CNKI. The focus was on methcathinone and its neuropsychological disorders and physical health complications, specifically in adult offspring.Result: A total of 8 studies met the inclusion criteria, resulting in a dataset of methcathinone on neurobehavioral and cognitive functions. These studies mainly found that prenatal methcathinone exposure in rats led to delayed physical development and induced anxiety-like behavior in offspring, with changes observed in neurobehavioral tests and the concentration of serotonin and dopamine. Furthermore, neurochemical effects were identified, showing dose- and time-dependent increases in extracellular dopamine and serotonin concentrations, and neurotoxic potential towards brain dopamine neurons.Conclusion: This study concludes that methcathinone poses severe risks, including neurotoxicity for users and developmental harm for offspring, necessitating ongoing research to comprehend associated risks and inform public health interventions.","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143718275","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Deciphering T Cell Dynamics in Alzheimer's Disease Pathogenesis: Insights and Implications. 在阿尔茨海默病发病机制中解读T细胞动力学：见解和意义。

IF 4.8 2区医学

Current Neuropharmacology Pub Date : 2025-03-21 DOI: 10.2174/011570159X350611250303044527

Qiqi Yang, Yunjie Qiu, Junjun Ni, Hui Li, Hong Qing

{"title":"Deciphering T Cell Dynamics in Alzheimer's Disease Pathogenesis: Insights and Implications.","authors":"Qiqi Yang, Yunjie Qiu, Junjun Ni, Hui Li, Hong Qing","doi":"10.2174/011570159X350611250303044527","DOIUrl":"https://doi.org/10.2174/011570159X350611250303044527","url":null,"abstract":"Neuroinflammation has emerged as a crucial factor in the pathogenesis of Alzheimer's disease (AD), paving the way for promising therapeutic interventions. Increasing evidence highlights the interplay between the peripheral immune system and the central nervous system (CNS) in driving neuroinflammation, with T lymphocytes playing a vital role in both regulatory and effector functions. Aberrant activation of T cells during the early stages of neuroinflammation perpetuates inflammatory responses by interacting with CNS glial cells and releasing pro-inflammatory mediators, such as IFN-γ, TNF-α, and IL-17. Studies have documented significant T cell activation and infiltration into the brain parenchyma in AD, contributing to disease progression. However, the specific mechanisms by which T cells mediate AD pathogenesis remain unclear. This comprehensive review synthesizes the current understanding of T cell involvement in AD pathology, emphasizing their aberrant activation, interactions with microglia, tau protein pathology, and the influence of gut microbiota. Finally, we propose potential treatment modalities for AD, highlighting the promise of T cellbased therapies currently under investigation in clinical trials. Understanding the critical role of T cells in intercellular communication and disease progression may enhance our comprehension of the pathophysiology of AD.","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143699905","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Research Progress on Neural Cell Culture Systems. 神经细胞培养系统的研究进展。

IF 4.8 2区医学

Current Neuropharmacology Pub Date : 2025-03-12 DOI: 10.2174/011570159X360193250219082312

Ting Li, Xiaosong Qin, Qiang Ao

{"title":"Research Progress on Neural Cell Culture Systems.","authors":"Ting Li, Xiaosong Qin, Qiang Ao","doi":"10.2174/011570159X360193250219082312","DOIUrl":"https://doi.org/10.2174/011570159X360193250219082312","url":null,"abstract":"The nervous system, including the central nervous system and peripheral nervous system, has the most intricate structure and function among all systems in the human body. In studies of physiological and pathological functions, cell culture systems serve as an indispensable tool to simulate the nervous system in vivo. Two-dimensional (2D), three-dimensional (3D), and four-dimensional (4D) neural cell culture systems are used to assess the functional interconnectivity of neuronal tissues and have markedly advanced in recent years. Although 2D culture systems have predominated, they cannot accurately recapitulate the dynamic complexity of the in vivo environment, cell-cell communication, and nervous system structures. Consequently, studies have shifted to using 3D or 4D cell culture systems to achieve more realistic biochemical and biomechanical microenvironments. Nevertheless, many limitations persist in 3D or 4D culture systems, including difficulties in deciphering dynamic and reciprocal remodeling processes, as well as the spatiotemporal distributions of oxygen, nutrients, and metabolic waste. Here, we review 2D, 3D, and 4D culture systems, discuss the advantages and limitations of these techniques in modeling physiologically and pathologically relevant processes, and suggest directions for future research.","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143613863","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Prenatal Stress Increases the Risk of the FPR2-related Dysfunction in the Brain's Resolution of Inflammation: A Study on the Humanized APPNL-F/NL-F Mouse Model of Alzheimer's Disease. 产前应激增加大脑炎症解决中fpr2相关功能障碍的风险：人源化APPNL-F/NL-F阿尔茨海默病小鼠模型的研究

IF 4.8 2区医学

Current Neuropharmacology Pub Date : 2025-03-12 DOI: 10.2174/011570159X345385241004060055

Ewa Trojan, Jakub Frydrych, Władysław Lasoń, Agnieszka Basta-Kaim

{"title":"Prenatal Stress Increases the Risk of the FPR2-related Dysfunction in the Brain's Resolution of Inflammation: A Study on the Humanized APPNL-F/NL-F Mouse Model of Alzheimer's Disease.","authors":"Ewa Trojan, Jakub Frydrych, Władysław Lasoń, Agnieszka Basta-Kaim","doi":"10.2174/011570159X345385241004060055","DOIUrl":"https://doi.org/10.2174/011570159X345385241004060055","url":null,"abstract":"Introduction: Brain aging is a complex process involving genetic, neurodevelopmental, and environmental factors. Inherent features of this process are cellular senescence, the development of senescence-associated secretory phenotype (SASP), and prolonged inflammation.Methods: Recently, progress has been made in understanding the biological roles of FPR2 receptors and their ligands in the mechanism of inflammation resolution (RoI) in the brain. However, the number of studies comparing the influence of prenatal stress (PS) on RoI in physiological aging and neurodegenerative disorders pathology is very limited, and the data need to be more consistent. Here, we examined whether PS can condition the pattern of age-dependent cognitive and RoI changes in the prefrontal cortex and hippocampus in wild-type and hAPPNL-F/NL-F KI male mice.Results: We discovered that in aging, the memory deficits are accompanied by the limitation of the availability of pro-resolving FPR2 ligands, the rising proinflammatory microglia polarization, and inflammatory ligands mediated FPR2 overactivation. Moreover, the present study suggested the subtle role of the RoI deficits in creating brain cells' senescence and shifting the immunomodulators to the proinflammatory direction. PS has been revealed as a substantial factor modulating the profile of inflame-aging in a manner strongly determined by the age of animals and the brain structure under study, mainly in hAPPNL-F/NL-F KI male mice.Conclusion: Our results identify the FPR2 receptors as a driver regulating the RoI process in the brain and highlight that PS has diversified the picture of age-dependent neurodegenerative pathology.","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143613860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

ATP1A3 Acts as a Potential Anti-oncogene in Glioblastoma via the Antagonizing Interaction with Small Nuclear Ribonucleoprotein Polypeptide G. ATP1A3通过与小核糖核蛋白多肽G的拮抗作用在胶质母细胞瘤中发挥潜在的抗癌基因作用。

IF 4.8 2区医学

Current Neuropharmacology Pub Date : 2025-03-11 DOI: 10.2174/011570159X361656250128073206

Shuang Zou, Bing Qin, Qi Chen, Zhiwei Shen, Qichang Liu, Xiangdong Zhu, Yulong Lan

{"title":"ATP1A3 Acts as a Potential Anti-oncogene in Glioblastoma via the Antagonizing Interaction with Small Nuclear Ribonucleoprotein Polypeptide G.","authors":"Shuang Zou, Bing Qin, Qi Chen, Zhiwei Shen, Qichang Liu, Xiangdong Zhu, Yulong Lan","doi":"10.2174/011570159X361656250128073206","DOIUrl":"https://doi.org/10.2174/011570159X361656250128073206","url":null,"abstract":"Background: The sodium pump α3 subunit (ATP1A3) is associated with various brain's physiological and pathological mechanisms. However, its molecular mechanisms and cellular targets in glioblastoma (GBM) are poorly understood.Methods: Bioinformatics and phosphor-proteomics analysis, target fishing experiment, confocal immunofluorescence, molecular cloning, and western blot techniques were carried out to elucidate probable downstream signaling pathways. Then GBM xenografts were established to assess potential molecular mechanisms of ATP1A3 associated with its in vivo anti-glioma impacts.Results: The mechanistic analyses indicated that the antagonism between ATP1A3 and small nuclear ribonucleoprotein polypeptide G (SNRPG) could suppress GBM growth. ATP1A3 inhibits SNRPGinduced GBM epithelial-mesenchymal transition, and SNRPG decreases ATP1A3 by increasing phosphorylation at S643. As a negative feedback loop, ATP1A3 overexpression causes a reduction of SNRPG-induced invasion-metastasis cascades via regulating KLF9. Furthermore, by using artificial intelligence (AI) techniques, we have also exerted the design and application of a synthetic peptide (ATP1A3-S643 peptide), which could be the potential inhibitor of ATP1A3 phosphorylation. To better explore the anti-glioma effect of ATP1A3 activation, a bioengineering nanomedicine capable of ondemand ATP1A3 activator delivery to the brain for GBM has also been developed in this work, which exhibited an improved therapeutic efficacy in the ATP1A3-targeted treatment of glioma.Conclusion: ATP1A3 is a potential anti-glioma treatment target, and its activation critically depends on its antagonizing interaction with SNRPG.","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604128","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Advances and Challenges in Traumatic Brain Injury from a Forensic Perspective. 从法医角度看外伤性脑损伤的进展与挑战。

IF 4.8 2区医学

Current Neuropharmacology Pub Date : 2025-02-26 DOI: 10.2174/011570159X352125241031030110

Shu-Quan Zhao, Yan-Wei Shi, Xiao-Guang Wang, Ke Liu, Hu Zhao

引用次数: 0

Roles of Microglia in Synaptogenesis, Synaptic Pruning, and Synaptic Plasticity in Physiological Conditions and Central Nervous System Disorders. 小胶质细胞在生理状况和中枢神经系统疾病中的突触生成、突触修剪和突触可塑性中的作用。

IF 4.8 2区医学

Current Neuropharmacology Pub Date : 2025-02-26 DOI: 10.2174/1570159X23666250225091729

Meizhen Xie, Tian Wang, Jiachun Feng, Di Ma, Liangshu Feng, Yulei Hao

{"title":"Roles of Microglia in Synaptogenesis, Synaptic Pruning, and Synaptic Plasticity in Physiological Conditions and Central Nervous System Disorders.","authors":"Meizhen Xie, Tian Wang, Jiachun Feng, Di Ma, Liangshu Feng, Yulei Hao","doi":"10.2174/1570159X23666250225091729","DOIUrl":"https://doi.org/10.2174/1570159X23666250225091729","url":null,"abstract":"Microglia are resident immune cells in the brain that have been widely studied for their immune surveillance and phagocytosis. In recent years, the important role of microglia in synapse formation, elimination, and plasticity is gradually being recognized. Synapses are the main communication mode between neurons. They undergo constant changes in quantity and plasticity throughout the life cycle, which is the basis of learning and memory. Microglia are highly motile, branched forms that monitor the microenvironment of the central nervous system (CNS) and promote synapse formation and maturation. They recognize and phagocytose redundant synapses through specific phagocytosis receptors. Furthermore, microglia regulate synaptic plasticity by releasing various effectors. The roles of microglia on synapses ensure the proper function of neural networks. Synaptic dysfunction and microglia activation are common features in CNS disorders, such as Alzheimer's disease, Parkinson's disease, ischemic stroke, cerebral hemorrhage, traumatic brain injury, multiple sclerosis, and epilepsy. Highly heterogeneous microglia exhibit diverse functions in these diseases and participate in disease progression by exacerbating or inhibiting synaptic dysfunction, in addition to neuroimmune and inflammation. In this article, we summarize the role of microglia on synapses under physiological conditions and in CNS disorders. We highlight the possible mechanisms by which microglia regulate synapse function in CNS disorders and how this affects the progression of the diseases. We aim to explore potential therapeutic targets for CNS disorders.","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514981","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Beneficial and Detrimental Effects of Uric Acid on Alzheimer's Disease. 尿酸对阿尔茨海默病的有益和有害影响。

IF 4.8 2区医学

Current Neuropharmacology Pub Date : 2025-02-18 DOI: 10.2174/011570159X349365250128072146

O V Tovchiga, I Inkielewicz-Stepniak

{"title":"Beneficial and Detrimental Effects of Uric Acid on Alzheimer's Disease.","authors":"O V Tovchiga, I Inkielewicz-Stepniak","doi":"10.2174/011570159X349365250128072146","DOIUrl":"https://doi.org/10.2174/011570159X349365250128072146","url":null,"abstract":"The interconnection between brain function and hyperuricemia remains controversial since the available evidence indicates both the potent neuroprotective role of uric and its negative cardiovascular and metabolic effects, possible prooxidant activity. A mixed (protective and risk) effect of uric acid on neurological disorders was assumed. Among the neurodegenerative diseases, Alzheimer's disease remains the most prevalent, causes disability, and lacks highly effective treatments. Therefore, this review aims to delineate the beneficial and detrimental effects of uric acid on Alzheimer's disease. This can not only facilitate estimating the benefits and risks of urate-lowering or urate-increasing interventions in different conditions but also can enhance understanding of the molecular pathways associated with the protective role of uric acid, leading to the identification of new therapeutic targets for neuroprotection. Firstly, we addressed interconnections between UA and AD in different patients and population subgroups. Secondly, we analysed which differences can arise at the level of uric acid transport to the brain, its influence on BBB, and its presence in brain tissue and cerebrospinal fluid. Such aspects as xanthine oxidase interrelationship with the risk of cognitive impairment was elucidated, as well as the unexpected interconnection between uric acid exchange and the cholinergic system. Finally, an analysis was done of the beneficial and detrimental effects of uric acid on such targets of Alzheimer's disease pathogenesis as the amyloid-β pathway, proinflammatory markers, peroxynitrite scavenging, and other aspects of prooxidant-antioxidant status.","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143457181","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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 Modulatory Effects of Anesthetics and Analgesics on Neurophysiological Monitoring and Underlying Mechanisms. 麻醉药和镇痛药对神经生理监测的调节作用及其机制。

IF 4.8 2区医学

Current Neuropharmacology Pub Date : 2025-02-18 DOI: 10.2174/011570159X349119250127104107

Yu Leng, Yi Teng, Jin Liu, Xian Zou, Mengchan Ou, Tao Zhu, Peng Liang, Cheng Zhou

{"title":"The Modulatory Effects of Anesthetics and Analgesics on Neurophysiological Monitoring and Underlying Mechanisms.","authors":"Yu Leng, Yi Teng, Jin Liu, Xian Zou, Mengchan Ou, Tao Zhu, Peng Liang, Cheng Zhou","doi":"10.2174/011570159X349119250127104107","DOIUrl":"https://doi.org/10.2174/011570159X349119250127104107","url":null,"abstract":"Intraoperative Neurophysiological Monitoring (IONM) is an indispensable surgical tool that offers invaluable insights into neurological function across a spectrum of anatomical areas. By comprehensively assessing the integrity of the brain, brainstem, spinal cord, cranial nerves, and peripheral nerves, IONM plays a pivotal role in guiding surgical decision-making and optimizing patient outcomes, particularly in the context of high-risk procedures. Intraoperative drugs, especially anesthetics and/or analgesics, differentially modulate neurophysiological monitoring, which remarkably affects the application of neurophysiological monitoring under specific conditions and indicates the neurobiological mechanisms of anesthetics/analgesics. This review will describe various neurophysiological modalities utilized in intraoperative procedures, each employing a wide variety of physiological principles; summarize the modulatory effects of anesthetics/analgesics on these neurophysiological monitoring parameters; and elucidate their underlying mechanisms, with a particular emphasis on evoked potentials. Insights gleaned from this review can inform strategies of anesthesia management for surgeries that require IONM and guide future investigations on the mechanisms of anesthesia/analgesia.","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143456658","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Effects of a Rosiridin against Rotenone-induced Rats' Model of Parkinson's Disease: In-vivo Study and in silico Molecular Modeling. 罗西瑞定对鱼藤酮诱导的大鼠帕金森病模型的影响：体内研究和硅分子模型。

IF 5.3 2区医学

Current Neuropharmacology Pub Date : 2025-02-13 DOI: 10.2174/011570159X349553250126050134

Misbahuddin Rafeeq, Fahad A Al-Abbasi, Muhammad Afzal, Khalid Saad Alharbi, Ehssan Moglad, Salwa D Al-Qahtani, Hussam A Bukhari, Faisal Imam, Nadeem Sayyed, Imran Kazmi

{"title":"Effects of a Rosiridin against Rotenone-induced Rats' Model of Parkinson's Disease: In-vivo Study and in silico Molecular Modeling.","authors":"Misbahuddin Rafeeq, Fahad A Al-Abbasi, Muhammad Afzal, Khalid Saad Alharbi, Ehssan Moglad, Salwa D Al-Qahtani, Hussam A Bukhari, Faisal Imam, Nadeem Sayyed, Imran Kazmi","doi":"10.2174/011570159X349553250126050134","DOIUrl":"10.2174/011570159X349553250126050134","url":null,"abstract":"Aim: The investigation aimed to study the outcome of rosiridin in Parkinson's disease (PD) induced by rotenone (ROT) in rodents.Methods: Rodents were randomized into IV groups and were induced with ROT followed by treatment with rosiridin. Group I-IV received saline as a vehicle, II-ROT (0.5 mg/kg S.C) for 28 consecutive days, III and IV- rosiridin 10 and 20 mg/kg orally with ROT. On completion of the experimental duration, behavioral investigations were carried out. Biochemical variables such as acetylcholinesterase (AChE), oxidative stress and antioxidants markers (Malondialdehyde-MDA, glutathione-GSH, superoxide dismutase-SOD, and catalase-CAT), anti-inflammatory (Interleukin-1 beta-IL-1β, IL-6, and tumor necrosis factor alpha-TNF-α), alteration in neurotransmitters (Serotonin-5-HT), norepinephrine, and dopamine-DA, along with metabolites such as 5-hydroxy indole acetic acid-5- HIAA),), mitochondrial complex I, II, IV, and caspase-3 activity were evaluated at the end of the experiment. Furthermore, molecular docking and dynamics were performed for target ligands.Results: Rosiridin significantly restored the level of AChE, oxidative stress and antioxidants markers (MDA, GSH, SOD, and CAT), anti-inflammatory (IL-1β, IL-6, and TNF-α), alteration in neurotransmitters, mitochondrial complex I, II, IV, and caspase-3 activity. Rosiridin has a favorable negative binding affinity to AChE (-8.99 kcal/mol). The results of the molecular dynamics simulations indicate that proteins undergo a substantial change in conformational dynamics when binding to rosiridin.Conclusion: In this study, rosiridin may exhibit neuroprotective properties against the Parkinson's model for treating PD.","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12272089/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143413716","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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