Neurochemical Research最新文献_第4页

Dual Targeting of TLR9 and cGAS-STING Pathways Attenuates Astrocyte Inflammatory Activation: Potential Implication in Multiple Sclerosis TLR9和cGAS-STING通路的双重靶向可减弱星形胶质细胞炎症激活：在多发性硬化症中的潜在意义

IF 3.8 3区医学

Neurochemical Research Pub Date : 2025-09-05 DOI: 10.1007/s11064-025-04529-1

Wenjun Shao, Xuejing Huo, Xiaoni Liu, Qian Zhang, Xiaodi Hao, Jiewen Zhang

{"title":"Dual Targeting of TLR9 and cGAS-STING Pathways Attenuates Astrocyte Inflammatory Activation: Potential Implication in Multiple Sclerosis","authors":"Wenjun Shao, Xuejing Huo, Xiaoni Liu, Qian Zhang, Xiaodi Hao, Jiewen Zhang","doi":"10.1007/s11064-025-04529-1","DOIUrl":"10.1007/s11064-025-04529-1","url":null,"abstract":"<div><p>This study aims to investigate the role of Toll-like receptor 9 (TLR9), a deoxyribose nucleic acid (DNA) sensor, in astrocyte activation and its contribution to multiple sclerosis (MS) pathogenesis. Additionally, we examined whether TLR9 and the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathways act synergistically to promote astrocyte inflammatory activation and whether combined inhibition of both pathways offers superior protective effects. Human astrocytes were treated with unmethylated Cytosine-phosphorothioate-guanine (CpG) oligodeoxynucleotides at varying concentrations. Intervention groups included treatment with a TLR9 blocker (anti-TLR9) and a STING inhibitor (RU.521). Cellular responses were assessed by cell counting kit (CCK)-8 viability assay and Annexin V-based apoptosis detection. Enzyme-linked immunosorbent assay (ELISA) was used to quantify the secreted levels of lactate dehydrogenase (LDH), tumor necrosis factor (TNF)-α, and interleukins (IL)-6, IL-1β, and IL-18. Protein expression levels of TLR9, nuclear factor kappa B (NF-κB), phosphorylated NF-κB (p-NF-κB), STING, and cGAS were analyzed by Western blot. Treatment with unmethylated CpG oligodeoxynucleotides significantly reduced astrocyte viability and promoted apoptosis, while upregulating the expression of TLR9, p-NF-κB, and STING proteins. Combined treatment with both the TLR9 blocker and the STING inhibitor significantly restored cell viability, reduced apoptosis, and decreased the production of inflammatory factors in astrocytes. These findings suggest that targeting TLR9 and the STING pathway can alleviate astrocyte overactivation, indicating a potential therapeutic role for targeting the TLR9-cGAS-STING pathway in MS pathogenesis.</p></div>","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144990355","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}

引用次数: 0

Astrocyte Autophagy in Neurodegenerative Diseases: Current Progress in Mechanisms and Therapeutics 神经退行性疾病中的星形细胞自噬：机制和治疗的最新进展

IF 3.8 3区医学

Neurochemical Research Pub Date : 2025-09-05 DOI: 10.1007/s11064-025-04532-6

Jialei Qian, Shengyuan Ren, Tianning Ren, Renke Shi, Liang Qiao, Jing Kang

{"title":"Astrocyte Autophagy in Neurodegenerative Diseases: Current Progress in Mechanisms and Therapeutics","authors":"Jialei Qian, Shengyuan Ren, Tianning Ren, Renke Shi, Liang Qiao, Jing Kang","doi":"10.1007/s11064-025-04532-6","DOIUrl":"10.1007/s11064-025-04532-6","url":null,"abstract":"<div><p>Astrocytes, the most abundant and functionally diverse glial cell type in the brain, play a crucial role in maintaining cellular homeostasis and promoting neuronal survival. Autophagy is the process of transferring senescent, denatured, or damaged proteins and organelles from cells to lysosomes for degradation. However, recent research on autophagy in the central nervous system has focused on neurons. In this paper, we reviewed the latest findings on astrocyte autophagy and its mechanisms in regulating neurodegenerative disorders. It influences the pathological processes of Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and other synucleinopathies (including dementia with Lewy bodies and Parkinson’s disease dementia) by regulating oxidative stress and inflammatory responses, as well as aberrant protein aggregation and folding. Furthermore, we listed medications that can prevent or treat neurodegenerative disorders by modulating astrocyte autophagy pathways, providing new insights into preventive and therapeutic strategies for neurodegenerative diseases.</p></div>","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144990356","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}

引用次数: 0

A Journey between Neurons and Astrocytes: A Tribute to Giorgio Carmignoto 神经元和星形胶质细胞之间的旅程：致敬乔治·卡米诺托

IF 3.8 3区医学

Neurochemical Research Pub Date : 2025-09-04 DOI: 10.1007/s11064-025-04527-3

Micaela Zonta, Stefano Vicini, Nicoletta Berardi, Lamberto Maffei, Gian Michele Ratto, Paulo J. Magalhães, Tommaso Fellin, Gabriele Losi, Marta Gómez-Gonzalo, Alexei Verkhratsky

{"title":"A Journey between Neurons and Astrocytes: A Tribute to Giorgio Carmignoto","authors":"Micaela Zonta, Stefano Vicini, Nicoletta Berardi, Lamberto Maffei, Gian Michele Ratto, Paulo J. Magalhães, Tommaso Fellin, Gabriele Losi, Marta Gómez-Gonzalo, Alexei Verkhratsky","doi":"10.1007/s11064-025-04527-3","DOIUrl":"10.1007/s11064-025-04527-3","url":null,"abstract":"<div><p>The intimate relation between astrocytes and blood vessels was proposed by Camillo Golgi in 1870. Santiago Ramon y Cajal subsequently introduced the idea of astrocytes as regulators of functional hyperaemia accompanying neuronal activity in 1895. In 2003 Giorgio Carmignoto, Micaela Zonta, Tullio Pozzan and their colleagues revealed mechanisms of astrocytic control over vasodilatation. They demonstrated that astrocytic Ca<sup>2+</sup> signals are fundamental for translating neuronal activity into an increase of arterioles diameter, which in turn results in a local increase in the blood flow. This special issue celebrates the career of Giorgio, by gathering contributions of many friends of him, who will guide us along his scientific journey in this introductory paper, as well as presents original papers and reviews dedicated to astrocytes and their multiple functional role. It will become soon evident to the readers how, in every environment he has worked and lived, Giorgio developed strong relationships with people, always with the strong belief in the crucial role of collaborative effort in science, as well as in the value of friendship in life.</p></div>","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144934744","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}

引用次数: 0

Prognostic Value of MCM3AP-AS1 in Glioma and its Regulatory Effect on Tumor Progression MCM3AP-AS1在胶质瘤中的预后价值及其对肿瘤进展的调节作用

IF 3.8 3区医学

Neurochemical Research Pub Date : 2025-09-04 DOI: 10.1007/s11064-025-04539-z

Kang Gao, Lina Song, Deying Niu

{"title":"Prognostic Value of MCM3AP-AS1 in Glioma and its Regulatory Effect on Tumor Progression","authors":"Kang Gao, Lina Song, Deying Niu","doi":"10.1007/s11064-025-04539-z","DOIUrl":"10.1007/s11064-025-04539-z","url":null,"abstract":"<div><p>Long non-coding RNAs (lncRNAs) have emerged as promising cancer biomarkers due to their stability and detectability. This study aimed to investigate the clinical significance and molecular mechanisms of lncRNA MCA3AP-AS1 in glioma. This study collected the clinical data from 177 glioma patients, and the expression of MCM3AP-AS1 was measured in glioma tissues and cell lines. Kaplan-Meier and COX regression analyses were employed to assess its prognostic value in glioma. In the mechanism study, bioinformatics prediction, correlation analysis, and dual-luciferase assays were conducted to validate the regulatory network involving MCM3AP-AS1, miR-23c, and PIK3R3. Functional experiments (CCK-8, Transwell assays, and Western blot) further determined the impact of MCM3AP-AS1 on glioma cell functions and confirmed the potential regulatory mechanism. Upregulation of MCM3AP-AS1 in glioma was related to the WHO grade, KFS scores, and glioma poor prognosis. Correlation analysis, binding site prediction, and the dual-luciferase reporter assay confirmed the interaction relationship among MCM3AP-AS1, miR-23c, and PIK3R3. In mechanism, MCM3AP-AS1 knockdown suppressed the glioma cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT). This attenuated effect of downregulated MCM3AP-AS1 expression in glioma cell proliferation, migration, and invasion could be further reversed by miR-23c inhibition. Upregulated MCM3AP-AS1 expression in glioma was associated with the poor prognosis of glioma. MCM3AP-AS1 may promote glioma progression by enhancing cell proliferation, migration, and invasion through the miR-23c/PIK3R3 axis.</p></div>","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144934655","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}

引用次数: 0

Wnt7b Promotes Axon Differentiation and Extension by Regulating JNK-Mediated Cytoskeletal Dynamics Wnt7b通过调节jnk介导的细胞骨架动力学促进轴突分化和延伸

IF 3.8 3区医学

Neurochemical Research Pub Date : 2025-09-04 DOI: 10.1007/s11064-025-04540-6

Lorena P Neila, Sebastian Luna, Rodrigo Vena, Silvana B Rosso

{"title":"Wnt7b Promotes Axon Differentiation and Extension by Regulating JNK-Mediated Cytoskeletal Dynamics","authors":"Lorena P Neila, Sebastian Luna, Rodrigo Vena, Silvana B Rosso","doi":"10.1007/s11064-025-04540-6","DOIUrl":"10.1007/s11064-025-04540-6","url":null,"abstract":"<div><p>Neuronal polarization and axon growth are critical processes underlying neuronal differentiation and maturation. Wnt proteins have been implicated as key regulators of neuronal development; however, the cellular mechanisms through which they influence axon growth remain poorly understood. In this study, we investigated the role of Wnt7b in axon differentiation and elongation in hippocampal neurons, and aimed to characterize the underlying molecular mechanisms involved. Our results show that Wnt7b accelerates neuronal polarization and promotes axon elongation. In the presence of Wnt7b, most undifferentiated neurons polarized and subsequently developed longer axons compared to controls. Further analysis revealed that this effect is mediated by the JNK signaling pathway, as both pharmacological inhibition and expression of a dominant-negative JNK construct blocked Wnt7b-induced axonal elongation. Additionally, Wnt7b triggered local activation of JNK in growing axons and induced cytoskeletal rearrangements. Specially, Wnt stimulation promoted microtubule stabilization along newly formed axons and enhanced the protrusion of dynamic microtubules into the growth cones, a process that may facilitate axon extension. Together, these findings identify Wnt7b as a crucial modulator of axon differentiation and elongation, acting through activation of the JNK pathway.</p></div>","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144934654","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}

引用次数: 0

Autophagy Modulation by Antidepressants: Mechanisms and Implications 抗抑郁药物调节自噬：机制和意义

IF 3.8 3区医学

Neurochemical Research Pub Date : 2025-09-04 DOI: 10.1007/s11064-025-04534-4

Yuanzi Zheng, Yanjun Ma, Yuhang Pan, Tahir Ali, Chengyou Zheng, Kelvin Kaikei Miu, Zhangting Wang, Limeng Zhang, Shupeng Li, Zhen Tan

{"title":"Autophagy Modulation by Antidepressants: Mechanisms and Implications","authors":"Yuanzi Zheng, Yanjun Ma, Yuhang Pan, Tahir Ali, Chengyou Zheng, Kelvin Kaikei Miu, Zhangting Wang, Limeng Zhang, Shupeng Li, Zhen Tan","doi":"10.1007/s11064-025-04534-4","DOIUrl":"10.1007/s11064-025-04534-4","url":null,"abstract":"<div><p>Depression is a significant global health concern that extends beyond mere neurotransmitter imbalances, as the significance of autophagy in cellular recycling is increasingly recognized as pivotal in its pathogenesis and therapeutic intervention. This review thoroughly integrates the insights on how various antidepressants, such as SSRIs, SNRIs, and TCAs, confer therapeutic efficacy through modulation of autophagy pathways. We present evidence indicating that these pharmacological agents can augment autophagic flux, facilitate the clearance of neurotoxic protein aggregates, mitigate neuroinflammation, and enhance mitochondrial functionality, all of which represent critical elements of depressive pathology. While acknowledging the context-dependent effects across varying neuronal populations and phases of the disorder, we delineate promising therapeutic targets within the autophagy framework (e.g., ULK1/Beclin-1 initiation complex, TFEB-mediated lysosomal biogenesis). Furthermore, we confront existing translational challenges, underscoring the necessity for insights that are specific to distinct cell types and clinically pertinent biomarkers of autophagy. This review promotes a paradigm shift towards precision psychiatry, accentuating the significance of individualized treatment strategies informed by autophagy profiling. By linking foundational mechanistic insights, we establish targeted autophagy modulation as a revolutionary pathway for developing more effective and personalized interventions for depressive disorders.</p><h3>Graphical Abstract</h3><div><figure><div><div><picture><source><img></source></picture></div></div></figure></div></div>","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144934656","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}

引用次数: 0

Hindbrain Lactoprivic Regulation of Hypothalamic Third Ventricular Alpha-2 Tanycyte Metabolic Sensor Gene Expression in Hypoglycemic Male Versus Female Rats 低血糖雌雄大鼠下丘脑第三脑室α -2伸长细胞代谢传感器基因表达的后脑乳腔调节

IF 3.8 3区医学

Neurochemical Research Pub Date : 2025-09-04 DOI: 10.1007/s11064-025-04533-5

Rajesh K. Yadav, Subash Sapkota, Karen P. Briski

{"title":"Hindbrain Lactoprivic Regulation of Hypothalamic Third Ventricular Alpha-2 Tanycyte Metabolic Sensor Gene Expression in Hypoglycemic Male Versus Female Rats","authors":"Rajesh K. Yadav, Subash Sapkota, Karen P. Briski","doi":"10.1007/s11064-025-04533-5","DOIUrl":"10.1007/s11064-025-04533-5","url":null,"abstract":"<div><p>Alpha-2 (α2-) tanycytes line the ventral wall of the third ventricle where they ostensibly engage in metabolic screening. The oxidizable glycolytic end-product L-lactate is a gauge of hindbrain energy stability that is imparted to forebrain glucose-regulatory loci by norepinephrine signaling. Current research used a validated whole-animal model for insulin-induced hypoglycemia (IIH) to address the premise that hindbrain lactate status imposes sex-specific control of eu- and/or hypoglycemic patterns of α2-tanycyte chemosensor gene transcription in vivo. Vimentin-immunopositive α2-tanycytes were laser-catapult-microdissected from male and female brain sections after subcutaneous insulin injection and caudal fourth ventricular (CV4) L-lactate- or vehicle infusion for single-cell multiplex qPCR analysis of glucose and energy sensor gene expression. Hindbrain lactate infusion reversed IIH repression of α2-tanycyte glucose transporter-2 mRNA in females and amplified (males) or reversed (females) up-regulated glucokinase gene transcription. Lactate increased α2-tanycyte ATP-sensitive potassium channel Kir6.2 mRNA levels in hypoglycemic rats of each sex, reversing transcriptional inhibition in males or amplifying up-regulated expression in females. In both sexes, IIH-associated down-regulation of energy sensor 5’-AMP-activated protein kinase catalytic subunit isoforms alpha-1 and − 2 gene profiles was correspondingly unaffected or reversed by lactate. Hypoglycemia increased or decreased α2-tanycyte alpha<sub>1a</sub> and beta<sub>1</sub> receptor mRNA content, respectively; lactate caused opposite, sex-specific adjustments in transcriptional reactivity of the former gene yet did not affect the latter profile in either sex. Results show that hypothalamic α2-tanycytes are direct target for norepinephrine stimulation and document sex-dimorphic hindbrain lactoprivic regulation of chemosensor gene transcriptional responses to in vivo hypoglycemia.</p></div>","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144934653","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}

引用次数: 0

Minocycline Protects Against Oxidative Stress in a Model of Maple Syrup Urine Disease 米诺环素在枫糖浆尿病模型中保护抗氧化应激

IF 3.8 3区医学

Neurochemical Research Pub Date : 2025-09-03 DOI: 10.1007/s11064-025-04549-x

Isabela da Silva Lemos, Rejane Figueiredo Seldenreich, Carolina Giassi Alano, Laura Quinsani Schmitt, Rafaela Tezza Matiola, Ellen De Pieri, Fabricia Petronilho, Ricardo Andrez Machado-De-Ávila, Emilio Luiz Streck

{"title":"Minocycline Protects Against Oxidative Stress in a Model of Maple Syrup Urine Disease","authors":"Isabela da Silva Lemos, Rejane Figueiredo Seldenreich, Carolina Giassi Alano, Laura Quinsani Schmitt, Rafaela Tezza Matiola, Ellen De Pieri, Fabricia Petronilho, Ricardo Andrez Machado-De-Ávila, Emilio Luiz Streck","doi":"10.1007/s11064-025-04549-x","DOIUrl":"10.1007/s11064-025-04549-x","url":null,"abstract":"<div><p>Branched-chain amino acids (BCAA) leucine, isoleucine, and valine are metabolized by complex branched-chain ketoacids dehydrogenase (BCKDH). In Maple Syrup Urine Disease (MSUD), the BCKDH complex has its activity blocked by a genetic mutation, compromising the BCAA metabolism and leading to the accumulation of these BCAA, related to neurological damage in this disease. Thus, minocycline is a broad-spectrum antibiotic, bacteriostatic, and studies have shown benefits in neurodegenerative disease progression, like reduction of oxidative stress, inflammation, and downregulation of molecular pathways, such as apoptosis. Therefore, we make the hypothesis that the minocycline can ameliorate oxidative stress in the MSUD model. For this, we used 7-day-old male rats, who were treated with BCAA (leucine 393.42 mg/kg, isoleucine 121.66 mg/kg and valine 126.4 mg/kg) or saline solution (0,9%) subcutaneously, water, or minocycline (50 mg/kg) via gavage. Our results show that the MSUD group presents an increase in DCFH oxidation and TBARS levels, as well as a decrease in sulfhydryl content, related to oxidative species production, lipid and protein damage, and minocycline treatment rescues this damage found. In antioxidant activity, we found an increase in SOD activity also, a decrease in CAT in all groups studied compared to the control group. So, our results present positive effects of minocycline in MSUD, showing a potential use in this disease; moreover, more studies are necessary to understand the role of this molecule in this disease.</p></div>","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144934743","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}

引用次数: 0

Evaluation of the Potential Anticonvulsant and Neuroprotective Effects of Ganoderma Lucidum Extract in an Animal Model of Pentylenetetrazol-Induced Seizures 灵芝提取物对戊四唑致癫痫动物模型的潜在抗惊厥和神经保护作用的评价

IF 3.8 3区医学

Neurochemical Research Pub Date : 2025-09-03 DOI: 10.1007/s11064-025-04536-2

Itto Rahou Abdessamad, El-Hessni Aboubaker, Bahbiti Youssef, Bikjdaouene Leila, Azeroil Fatima, El Mekhlouf Youssef, Ibouzine-Dine Laila, Mesfioui Abdelhalem

{"title":"Evaluation of the Potential Anticonvulsant and Neuroprotective Effects of Ganoderma Lucidum Extract in an Animal Model of Pentylenetetrazol-Induced Seizures","authors":"Itto Rahou Abdessamad, El-Hessni Aboubaker, Bahbiti Youssef, Bikjdaouene Leila, Azeroil Fatima, El Mekhlouf Youssef, Ibouzine-Dine Laila, Mesfioui Abdelhalem","doi":"10.1007/s11064-025-04536-2","DOIUrl":"10.1007/s11064-025-04536-2","url":null,"abstract":"<div><p>Ganoderma lucidum extract (GLE) has neuro-therapeutic and anticonvulsant effects. This study aimed to evaluate the potential neuroprotective and antioxidant effects of ethanolic extract on pentylenetetrazol-induced brain damage in male Wistar rats and to analyze behavioral manifestations in vivo. Seizure latency, duration, and severity were measured in PTZ-treated rats according to the Racine scale; thus, oxidative stress markers, malondialdehyde (MDA), nitric oxide (NO), and catalase catalytic activity were measured by the 2-thiobarbituric acid, Griess reagent, and hydrogen peroxide methods, respectively. PTZ-injured rats showed both shorter seizure latency and longer seizure duration and intense seizure severity. The effects were enhanced by GLE in a dose-dependent manner. In addition, GLE decreased NO levels, increased catalase levels and decreased MDA levels in the hippocampus and the prefrontal cortex in rats treated with PTZ (75 mg/kg; i.p.). GLE conferred anticonvulsant and neuroprotective effects against PTZ-induced brain damage by repressing molecular processes involved in the production of oxidative stress markers.</p><h3>Graphical Abstract</h3><div><figure><div><div><picture><source><img></source></picture></div></div></figure></div></div>","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144934742","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}

引用次数: 0

Alamandine Rescues Cognitive Impairment and Ameliorates Alzheimer’s Disease-Like Neuropathology in APP/PS1 Mice Alamandine拯救APP/PS1小鼠的认知障碍和改善阿尔茨海默病样神经病理

IF 3.8 3区医学

Neurochemical Research Pub Date : 2025-08-25 DOI: 10.1007/s11064-025-04531-7

Shiyao Wang, Zhaohan Xu, Siyu Wang, Qiang Peng, Siqi Zhu, Caidong Liu, Yingdong Zhang, Rui Duan

{"title":"Alamandine Rescues Cognitive Impairment and Ameliorates Alzheimer’s Disease-Like Neuropathology in APP/PS1 Mice","authors":"Shiyao Wang, Zhaohan Xu, Siyu Wang, Qiang Peng, Siqi Zhu, Caidong Liu, Yingdong Zhang, Rui Duan","doi":"10.1007/s11064-025-04531-7","DOIUrl":"10.1007/s11064-025-04531-7","url":null,"abstract":"<div><p>Alzheimer’s disease (AD) is on the rise worldwide, consequently driving a growing demand for effective prevention and treatment strategies. Alamandine is a member of the renin–angiotensin system family. Although alamandine exhibits protective effects in the pathophysiology of various disorders, its role in AD remains an unexplored area. This research aims to elucidate the benefits and mechanisms of alamandine in an in vivo model of AD. The mice received intracerebroventricular injections of vehicle or alamandine once daily for 4 weeks. The Morris water maze was conducted to assess spatial learning ability. Nissl staining was performed to evaluate neuronal injury. Important inflammation indictors were detected both by qRT-PCR and ELISA. Representative oxidative stress indicators and Fe<sup>2+</sup> levels were measured using corresponding assay kits. Western blot was employed to detect the expression levels of the related proteins. We found that alamandine mitigates cognitive function and spatial learning impairment in APP/PS1 mice. Alamandine shows positive therapeutic effects by ameliorating the phosphorylation of tau proteins and suppressing neuroinflammation. In addition, alamandine mitigates the oxidative stress, ferroptosis and endoplasmic reticulum stress (ERS) in the brain of APP/PS1 mice. Our research indicates that alamandine alleviates cognitive impairment in APP/PS1 mice and inhibits inflammation, oxidative stress, ferroptosis, and ERS. It may serve as a promising approach to alleviate symptoms and promote remission in AD.</p></div>","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144894001","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}

引用次数: 0