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Emerging Trends: Neurofilament Biomarkers in Precision Neurology 新趋势:精准神经学中的神经丝生物标记。
IF 3.7 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-30 DOI: 10.1007/s11064-024-04244-3
Priti Sharma, Aditi Giri, Prabhash Nath Tripathi

Neurofilaments are structural proteins found in the cytoplasm of neurons, particularly in axons, providing structural support and stability to the axon. They consist of multiple subunits, including NF-H, NF-M, and NF-L, which form long filaments along the axon’s length. Neurofilaments are crucial for maintaining the shape and integrity of neurons, promoting axonal transport, and regulating neuronal function. They are part of the intermediate filament (IF) family, which has approximately 70 tissue-specific genes. This diversity allows for a customizable cytoplasmic meshwork, adapting to the unique structural demands of different tissues and cell types. Neurofilament proteins show increased levels in both cerebrospinal fluid (CSF) and blood after neuroaxonal damage, indicating injury regardless of the underlying etiology. Precise measurement and long-term monitoring of damage are necessary for determining prognosis, assessing disease activity, tracking therapeutic responses, and creating treatments. These investigations contribute to our understanding of the importance of proper NF composition in fundamental neuronal processes and have implications for neurological disorders associated with NF abnormalities along with its alteration in different animal and human models. Here in this review, we have highlighted various neurological disorders such as Alzheimer’s, Parkinson’s, Huntington’s, Dementia, and paved the way to use neurofilament as a marker in managing neurological disorders.

神经丝是神经元细胞质中的结构蛋白,尤其是在轴突中,为轴突提供结构支持和稳定性。它们由多个亚基组成,包括 NF-H、NF-M 和 NF-L,沿着轴突的长度形成长丝。神经丝对于维持神经元的形状和完整性、促进轴突运输和调节神经元功能至关重要。它们是中间丝(IF)家族的一部分,该家族有大约 70 个组织特异性基因。这种多样性使得细胞质网状结构可以定制,以适应不同组织和细胞类型的独特结构需求。神经轴受损后,脑脊液(CSF)和血液中的神经丝蛋白水平都会升高,这表明损伤与潜在病因无关。精确测量和长期监测损伤对于确定预后、评估疾病活动、跟踪治疗反应和创造治疗方法都是必要的。这些研究有助于我们了解适当的 NF 组成在神经元基本过程中的重要性,并对与 NF 异常及其在不同动物和人体模型中的改变有关的神经系统疾病产生影响。在这篇综述中,我们重点介绍了阿尔茨海默氏症、帕金森氏症、亨廷顿氏症、痴呆症等各种神经系统疾病,并为使用神经丝作为神经系统疾病的标记物铺平了道路。
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引用次数: 0
Sodium Butyrate Ameliorates Postoperative Delirium by Regulating Gut Microbiota Dysbiosis to Inhibit Astrocyte Activation in Aged Mice 丁酸钠通过调节肠道微生物群失衡抑制老年小鼠的星形胶质细胞活化来改善术后谵妄
IF 3.7 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-28 DOI: 10.1007/s11064-024-04245-2
Fanning Xu, Hui Chen, Yubo Gao, Xiaoxia Yang, Chun Zhang, Xinli Ni

Postoperative delirium (POD) is a common complication in elderly surgical patients, with limited targeted interventions due to incomplete understanding of its pathophysiological mechanisms. Central nervous system (CNS) inflammation, involving glial cell activation, particularly astrocytes, is considered crucial in POD development. Butyrate, a four-carbon fatty acid, has shown protective effects in CNS diseases, but its potential in mitigating POD remains unclear. This study aimed to investigate the impact of sodium butyrate on POD in aged mice. Behavioral tests, including open field, Y maze, and food burying tests, demonstrated that sodium butyrate preconditioning ameliorated laparotomy-induced delirium in aged mice. Pre-treatment with sodium butyrate inhibited astrocyte activation in the hippocampus, reduced interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) expression levels, and protected hippocampal neurons. Furthermore, the study revealed a connection between gut microbiota regulation and central neuroprotective effects mediated by astrocyte activation inhibition. Sodium butyrate improved the intestinal morphological barrier by rebalancing gut microbiota, inhibiting Proteobacteria and Actinobacteria, reducing Allobaculum and Bacteroides abundance, and increasing Oscillospira abundance. This regulation decreased gut permeability, limiting the entry of toxic substances into the bloodstream, thereby reducing inflammation spread and astrocyte overactivation, leading to central anti-inflammatory effects. In conclusion, sodium butyrate may ameliorate POD by inhibiting astrocyte-mediated neuroinflammation through gut microbiota rebalancing.

术后谵妄(POD)是老年手术患者常见的并发症,由于对其病理生理机制了解不全面,有针对性的干预措施十分有限。中枢神经系统(CNS)炎症涉及神经胶质细胞(尤其是星形胶质细胞)的激活,被认为是 POD 发生的关键因素。丁酸盐是一种四碳脂肪酸,对中枢神经系统疾病有保护作用,但其缓解 POD 的潜力仍不清楚。本研究旨在探讨丁酸钠对老年小鼠 POD 的影响。行为测试(包括开阔地、Y迷宫和食物掩埋测试)表明,丁酸钠预处理可改善老年小鼠腹腔镜手术诱发的谵妄。丁酸钠预处理抑制了海马星形胶质细胞的活化,降低了白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)的表达水平,并保护了海马神经元。此外,该研究还揭示了肠道微生物群调节与抑制星形胶质细胞活化所介导的中枢神经保护效应之间的联系。丁酸钠通过重新平衡肠道微生物群、抑制变形杆菌和放线菌、降低嗜球菌和嗜乳球菌的丰度以及增加鞘翅菌的丰度来改善肠道形态屏障。这种调节降低了肠道的通透性,限制了有毒物质进入血液,从而减少了炎症的扩散和星形胶质细胞的过度激活,产生了中枢抗炎作用。总之,丁酸钠可通过重新平衡肠道微生物群来抑制星形胶质细胞介导的神经炎症,从而改善 POD。
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引用次数: 0
Editorial Expression of Concern: The Possible Role of Brain-derived Neurotrophic Factor in Epilepsy 社论表达关注:脑源性神经营养因子在癫痫中的可能作用。
IF 3.7 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-27 DOI: 10.1007/s11064-024-04249-y
Raed AlRuwaili, Hayder M. Al-kuraishy, Ali I. Al-Gareeb, Naif H. Ali, Athanasios Alexiou, Marios Papadakis, Hebatallah M. Saad, Gaber El-Saber Batiha
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引用次数: 0
Zona Incerta GABAergic Neurons Facilitate Emergence from Isoflurane Anesthesia in Mice 昏迷区 GABA 能神经元有助于小鼠从异氟醚麻醉中苏醒。
IF 3.7 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-23 DOI: 10.1007/s11064-024-04230-9
Hong Chen, Chengxi Liu, Junxiao Liu, Chengdong Yuan, Haifeng He, Yu Zhang, Shouyang Yu, Tianyuan Luo, Wei Shen, Tian Yu

The zona incerta (ZI) predominantly consists of gamma-aminobutyric acid (GABAergic) neurons, located adjacent to the lateral hypothalamus. GABA, acting on GABAA receptors, serves as a crucial neuromodulator in the initiation and maintenance of general anesthesia. In this study, we aimed to investigate the involvement of ZI GABAergic neurons in the general anesthesia process. Utilizing in-vivo calcium signal optical fiber recording, we observed a decrease in the activity of ZI GABAergic neurons during isoflurane anesthesia, followed by a significant increase during the recovery phase. Subsequently, we selectively ablated ZI GABAergic neurons to explore their role in general anesthesia, revealing no impact on the induction of isoflurane anesthesia but a prolonged recovery time, accompanied by a reduction in delta-band power in mice under isoflurane anesthesia. Finally, through optogenetic activation/inhibition of ZI GABAergic neurons during isoflurane anesthesia, we discovered that activation of these neurons facilitated emergence without affecting the induction process, while inhibition delayed emergence, leading to fluctuations in delta band activity. In summary, these findings highlight the involvement of ZI GABAergic neurons in modulating the emergence of isoflurane anesthesia.

内侧区(ZI)主要由γ-氨基丁酸(GABA)能神经元组成,毗邻外侧下丘脑。GABA 作用于 GABAA 受体,是启动和维持全身麻醉的重要神经调节剂。本研究旨在探讨ZI GABA能神经元在全身麻醉过程中的参与情况。通过体内钙信号光纤记录,我们观察到在异氟烷麻醉过程中,ZI GABA能神经元的活性下降,随后在恢复阶段显著上升。随后,我们选择性地消融了ZI GABA能神经元,以探索它们在全身麻醉中的作用,结果显示,消融ZI GABA能神经元对异氟醚麻醉的诱导没有影响,但恢复时间延长,同时异氟醚麻醉下小鼠的δ波段功率降低。最后,通过在异氟烷麻醉期间对 ZI GABA 能神经元进行光遗传学激活/抑制,我们发现这些神经元的激活可促进苏醒而不影响诱导过程,而抑制则会延迟苏醒,从而导致δ波段活动的波动。总之,这些发现强调了ZI GABA能神经元参与调节异氟烷麻醉的唤醒。
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引用次数: 0
In Vivo Glucose Transporter-2 Regulation of Dorsomedial Versus Ventrolateral VMN Astrocyte Metabolic Sensor and Glycogen Metabolic Enzyme Gene Expression in Female Rat 体内葡萄糖转运体-2 对雌性大鼠背内侧血管网星形胶质细胞代谢传感器和糖原代谢酶基因表达的调控
IF 3.7 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-21 DOI: 10.1007/s11064-024-04246-1
Sagor C. Roy, Subash Sapkota, Madhu Babu Pasula, Karen P. Briski

Astrocyte glycogenolysis shapes ventromedial hypothalamic nucleus (VMN) regulation of glucostasis in vivo. Glucose transporter-2 (GLUT2), a plasma membrane glucose sensor, controls hypothalamic primary astrocyte culture glycogen metabolism in vitro. In vivo gene silencing tools and single-cell laser-catapult-microdissection/multiplex qPCR techniques were used here to examine whether GLUT2 governs dorsomedial (VMNdm) and/or ventrolateral (VMNvl) VMN astrocyte metabolic sensor and glycogen metabolic enzyme gene profiles. GLUT2 gene knockdown diminished astrocyte GLUT2 mRNA in both VMN divisions. Hypoglycemia caused GLUT2 siRNA-reversible up-regulation of this gene profile in the VMNdm, but down-regulated VMNvl astrocyte GLUT2 transcription. GLUT2 augmented baseline VMNdm and VMNvl astrocyte glucokinase (GCK) gene expression, but increased (VMNdm) or reduced (VMNvl) GCK transcription during hypoglycemia. GLUT2 imposed opposite control, namely stimulation versus inhibition of VMNdm or VMNvl astrocyte 5’-AMP-activated protein kinase-alpha 1 and -alpha 2 gene expression, respectively. GLUT2 stimulated astrocyte glycogen synthase (GS) gene expression in each VMN division. GLUT2 inhibited transcription of the AMP-sensitive glycogen phosphorylase (GP) isoform GP-brain type (GPbb) in each site, yet diminished (VMNdm) or augmented (VMNvl) astrocyte GP-muscle type (GPmm) mRNA. GLUT2 enhanced VMNdm and VMNvl glycogen accumulation during euglycemia, and curbed hypoglycemia-associated VMNdm glycogen depletion. Results show that VMN astrocytes exhibit opposite, division-specific GLUT2 transcriptional responsiveness to hypoglycemia. Data document divergent GLUT2 control of GCK, AMPK catalytic subunit, and GPmm gene profiles in VMNdm versus VMNvl astrocytes. Ongoing studies seek to determine how differential GLUT2 regulation of glucose and energy sensor function and glycogenolysis in each VMN location may affect local neuron responses to hypoglycemia.

星形胶质细胞糖原分解影响下丘脑腹内侧核(VMN)对体内葡萄糖稳态的调节。葡萄糖转运体-2(GLUT2)是一种质膜葡萄糖传感器,它在体外控制着下丘脑原代星形胶质细胞培养物的糖代谢。本研究利用体内基因沉默工具和单细胞激光-弹弓-微切片/多重 qPCR 技术来研究 GLUT2 是否控制背内侧(VMNdm)和/或腹外侧(VMNvl)VMN 星形胶质细胞代谢传感器和糖原代谢酶基因图谱。GLUT2基因敲除会减少两个VMN分部的星形胶质细胞GLUT2 mRNA。低血糖会导致 GLUT2 siRNA 在 VMNdm 中可逆地上调该基因谱,但会下调 VMNvl 星形胶质细胞 GLUT2 的转录。GLUT2 增加了基线 VMNdm 和 VMNvl 星形胶质细胞葡萄糖激酶(GCK)基因的表达,但在低血糖期间增加了(VMNdm)或减少了(VMNvl)GCK 的转录。GLUT2 对 VMNdm 或 VMNvl 星形胶质细胞 5'-AMP 激活的蛋白激酶-α 1 和-α 2 基因表达分别施加了相反的控制,即刺激与抑制。GLUT2 可刺激每个 VMN 分裂中星形胶质细胞糖原合成酶(GS)基因的表达。GLUT2 在每个部位都抑制了对 AMP 敏感的糖原磷酸化酶(GP)异构体 GP 脑型(GPbb)的转录,但却减少(VMNdm)或增加(VMNvl)了星形胶质细胞 GP 肌肉型(GPmm)的 mRNA。在优格血糖期间,GLUT2 增强了 VMNdm 和 VMNvl 的糖原累积,并抑制了低血糖相关的 VMNdm 糖原耗竭。研究结果表明,VMN 星形胶质细胞对低血糖表现出相反的、分部特异性的 GLUT2 转录反应。数据表明,在 VMNdm 和 VMNvl 星形胶质细胞中,GLUT2 对 GCK、AMPK 催化亚基和 GPmm 基因的控制存在差异。正在进行的研究试图确定 GLUT2 对葡萄糖和能量传感器功能以及糖原分解的不同调控在每个 VMN 位置可能会如何影响局部神经元对低血糖的反应。
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引用次数: 0
High-fat and High-sucrose Diet-induced Hypothalamic Inflammation Shows Sex Specific Features in Mice 高脂肪和高蔗糖饮食诱导的小鼠下丘脑炎症具有性别特征
IF 3.7 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-20 DOI: 10.1007/s11064-024-04243-4
Gabriela C. De Paula, Rui F. Simões, Alba M. Garcia-Serrano, João M. N. Duarte

Hypothalamic inflammation underlies diet-induced obesity and diabetes in rodent models. While diet normalization largely allows for recovery from metabolic impairment, it remains unknown whether long-term hypothalamic inflammation induced by obesogenic diets is a reversible process. In this study, we aimed at determining sex specificity of hypothalamic neuroinflammation and gliosis in mice fed a fat- and sugar-rich diet, and their reversibility upon diet normalization. Mice were fed a 60%-fat diet complemented by a 20% sucrose drink (HFHSD) for 3 days or 24 weeks, followed by a third group that had their diet normalized for the last 8 weeks of the study (reverse diet group, RevD). We determined the expression of pro- and anti-inflammatory cytokines, and of the inflammatory cell markers IBA1, CD68, GFAP and EMR1 in the hypothalamus, and analyzed morphology of microglia (IBA-1+ cells) and astrocytes (GFAP+ cells) in the arcuate nucleus. After 3 days of HFHSD feeding, male mice showed over-expression of IL-13, IL-18, IFN-γ, CD68 and EMR1 and reduced expression of IL-10, while females showed increased IL-6 and IBA1 and reduced IL-13, compared to controls. After 24 weeks of HFHSD exposure, male mice showed a general depression in the expression of cytokines, with prominent reduction of TNF-α, IL-6 and IL-13, but increased TGF-β, while female mice showed over-expression of IFN-γ and IL-18. Furthermore, both female and male mice showed some degree of gliosis after HFHSD feeding for 24 weeks. In mice of both sexes, diet normalization after prolonged HFHSD feeding resulted in partial neuroinflammation recovery in the hypothalamus, but gliosis was only recovered in females. In sum, HFHSD-fed mice display sex-specific inflammatory processes in the hypothalamus that are not fully reversible after diet normalization.

在啮齿动物模型中,下丘脑炎症是饮食诱发肥胖和糖尿病的基础。虽然饮食正常化在很大程度上使代谢损伤得以恢复,但肥胖饮食诱导的长期下丘脑炎症是否是一个可逆的过程仍是未知数。在这项研究中,我们旨在确定以富含脂肪和糖的饮食喂养的小鼠下丘脑神经炎症和胶质细胞病变的性别特异性,以及它们在饮食正常化后的可逆性。小鼠被喂食 60% 脂肪饮食并辅以 20% 蔗糖饮料(HFHSD)3 天或 24 周,第三组小鼠在研究的最后 8 周饮食正常化(反向饮食组,RevD)。我们测定了下丘脑中促炎症和抗炎症细胞因子以及炎症细胞标记物 IBA1、CD68、GFAP 和 EMR1 的表达,并分析了弓状核中小胶质细胞(IBA-1+ 细胞)和星形胶质细胞(GFAP+ 细胞)的形态。与对照组相比,喂食HFHSD 3天后,雄性小鼠的IL-13、IL-18、IFN-γ、CD68和EMR1过度表达,IL-10表达减少;雌性小鼠的IL-6和IBA1增加,IL-13减少。暴露于 HFHSD 24 周后,雄性小鼠的细胞因子表达普遍降低,TNF-α、IL-6 和 IL-13 明显减少,但 TGF-β 增加,而雌性小鼠的 IFN-γ 和 IL-18 则过度表达。此外,喂食HFHSD 24周后,雌性和雄性小鼠都出现了一定程度的神经胶质病变。在雌雄小鼠中,长期喂食HFHSD后饮食正常化可导致下丘脑部分神经炎症恢复,但只有雌性小鼠的神经胶质病变得到恢复。总之,喂食 HFHSD 的小鼠下丘脑显示出性别特异性炎症过程,这种过程在饮食正常化后并不能完全逆转。
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引用次数: 0
Ferulic Acid-Loaded Nanostructure Maintains Brain Levels of ACh, Glutamate, and GABA and Ameliorates Anxiety and Memory Impairments Induced by the d-Galactose Aging Process in Rats 阿魏酸负载的纳米结构可维持大鼠大脑中 ACh、谷氨酸和 GABA 的水平,并改善 D-半乳糖老化过程引起的焦虑和记忆损伤。
IF 3.7 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-20 DOI: 10.1007/s11064-024-04248-z
Domenika R. Rossato, Jéssica L. O. Rosa, Murilo B. Fontoura, Leana E. M. de Souza, Tielle M. de Almeida, Kathiane B. Kudrna, Scheila R. Schaffazick, Cristiane B. da Silva, Letícia Birk, Sarah Eller, Tiago F. de Oliveira, Marilise E. Burger

Population aging is a global reality driven by increased life expectancy. This demographic phenomenon is intrinsically linked to the epidemic of cognitive disorders such as dementia and Alzheimer's disease, posing challenges for elderly and their families. In this context, the search for new therapeutic strategies to prevent or minimize cognitive impairments becomes urgent, as these deficits are primarily associated with oxidative damage and increased neuroinflammation. Ferulic acid (FA), a natural and potent antioxidant compound, is proposed to be nanoencapsulated to target the central nervous system effectively with lower doses and an extended duration of action. Here, we evaluated the effects of the nanoencapsulated FA on d-galactose (d-Gal)- induced memory impairments. Male Wistar adult rats were treated with ferulic acid-loaded nanocapsules (FA-Nc) or non-encapsulated ferulic acid (D-FA) for 8 weeks concurrently with d-Gal (150 mg/kg s.c.) injection. As expected, our findings showed that d-Gal injection impaired memory processes and increased anxiety behavior, whereas FA-Nc treatment ameliorated these behavioral impairments associated with the aging process induced by d-Gal. At the molecular level, nanoencapsulated ferulic acid (FA-Nc) ameliorated the decrease in ACh and glutamate induced by d-galactose (d-Gal), and also increased GABA levels in the dorsal hippocampus, indicating its therapeutic superiority. Additional studies are needed to elucidate the mechanisms underlying our current promising outcomes. Nanoscience applied to pharmacology can reduce drug dosage, thereby minimizing adverse effects while enhancing therapeutic response, particularly in neurodegenerative diseases associated with aging. Therefore, the strategy of brain-targeted drug delivery through nanoencapsulation can be effective in mitigating aging-related factors that may lead to cognitive deficits.

Graphical Abstract

人口老龄化是预期寿命延长所导致的全球现实。这一人口现象与痴呆症和阿尔茨海默病等认知障碍的流行有着内在联系,给老年人及其家庭带来了挑战。在这种情况下,寻找新的治疗策略来预防或最大限度地减少认知障碍已成为当务之急,因为这些缺陷主要与氧化损伤和神经炎症加剧有关。阿魏酸(FA)是一种天然、强效的抗氧化化合物,有人建议将其纳米化,以更低的剂量和更长的作用时间有效地靶向中枢神经系统。在此,我们评估了纳米囊化 FA 对 d-半乳糖(d-Gal)诱导的记忆损伤的影响。雄性 Wistar 成年大鼠在注射 d-半乳糖(150 毫克/千克静脉注射)的同时,接受阿魏酸纳米胶囊(FA-Nc)或无胶囊阿魏酸(D-FA)治疗 8 周。正如预期的那样,我们的研究结果表明,注射d-Gal会损害记忆过程并增加焦虑行为,而FA-Nc治疗可改善这些与d-Gal诱导的衰老过程相关的行为损害。 在分子水平上,纳米阿魏酸胶囊(FA-Nc)可改善d-半乳糖(d-Gal)诱导的ACh和谷氨酸的减少,还可增加海马背侧的GABA水平,这表明它具有治疗优势。我们还需要进行更多的研究,以阐明目前取得的可喜成果背后的机制。将纳米科学应用于药理学可以减少药物剂量,从而最大限度地减少不良反应,同时提高治疗效果,尤其是在与衰老相关的神经退行性疾病方面。因此,通过纳米封装进行脑靶向给药的策略可以有效缓解可能导致认知障碍的衰老相关因素。
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引用次数: 0
Neuroprotective Properties of Coriander-Derived Compounds on Neuronal Cell Damage under Oxidative Stress-Induced SH-SY5Y Neuroblastoma and in Silico ADMET Analysis 芫荽提取物对氧化应激诱导的 SH-SY5Y 神经母细胞瘤神经细胞损伤的神经保护特性及硅学 ADMET 分析
IF 3.7 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-19 DOI: 10.1007/s11064-024-04239-0
Papitcha Jongwachirachai, Waralee Ruankham, Setthawut Apiraksattayakul, Saruta Intharakham, Veda Prachayasittikul, Wilasinee Suwanjang, Virapong Prachayasittikul, Supaluk Prachayasittikul, Kamonrat Phopin

An imbalance between reactive oxygen species (ROS) production and antioxidant defense driven by oxidative stress and inflammation is a critical factor in the progression of neurodegenerative diseases such as Alzheimer’s and Parkinson’s. Coriander (Coriandrum sativum L.), a culinary plant in the Apiaceae family, displays various biological activities, including anticancer, antimicrobial, and antioxidant effects. Herein, neuroprotective properties of three major bioactive compounds derived from coriander (i.e., linalool, linalyl acetate, and geranyl acetate) were investigated on hydrogen peroxide-induced SH-SY5Y neuroblastoma cell death by examining cell viability, ROS production, mitochondrial membrane potential, and apoptotic profiles. Moreover, underlying mechanisms of the compounds were determined by measuring intracellular sirtuin 1 (SIRT1) enzyme activity incorporated with molecular docking. The results showed that linalool, linalyl acetate, and geranyl acetate elicited their neuroprotection against oxidative stress via protecting cell death, reducing ROS production, preventing cell apoptosis, and modulating SIRT1 longevity. Additionally, in silico pharmacokinetic predictions indicated that these three compounds are drug-like agents with a high probability of absorption and distribution, as well as minimal potential toxicities. These findings highlighted the potential neuroprotective linalool, linalyl acetate, and geranyl acetate for developing alternative natural compound-based neurodegenerative therapeutics and prevention.

氧化应激和炎症导致的活性氧(ROS)生成与抗氧化防御之间的失衡是阿尔茨海默氏症和帕金森氏症等神经退行性疾病恶化的关键因素。芫荽(Coriandrum sativum L.)是繖形花科的一种烹饪植物,具有多种生物活性,包括抗癌、抗菌和抗氧化作用。本文通过研究过氧化氢诱导的 SH-SY5Y 神经母细胞瘤细胞的活力、ROS 生成、线粒体膜电位和凋亡谱,探讨了从芫荽中提取的三种主要生物活性化合物(即芳樟醇、乙酸芳樟酯和乙酸香叶酯)对神经的保护作用。此外,还通过测定细胞内 sirtuin 1(SIRT1)酶活性和分子对接来确定化合物的潜在机制。结果表明,芳樟醇、乙酸芳樟酯和乙酸香叶酯可通过保护细胞死亡、减少 ROS 生成、防止细胞凋亡和调节 SIRT1 的寿命,对氧化应激产生神经保护作用。此外,硅学药代动力学预测表明,这三种化合物是类药物,具有很高的吸收和分布概率,潜在毒性极低。这些发现突显了芳樟醇、乙酸芳樟酯和乙酸香叶酯具有潜在的神经保护作用,可用于开发基于天然化合物的神经退行性变治疗和预防替代品。
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引用次数: 0
Progress of Astrocyte-Neuron Crosstalk in Central Nervous System Diseases 中枢神经系统疾病中星形胶质细胞与神经元串联的研究进展
IF 3.7 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-18 DOI: 10.1007/s11064-024-04241-6
Yi Zhang, Ziyu Wang, Fenglian Xu, Zijun Liu, Yu Zhao, Lele Zixin Yang, Weirong Fang

Neurons are the primary cells responsible for information processing in the central nervous system (CNS). However, they are vulnerable to damage and insult in a variety of neurological disorders. As the most abundant glial cells in the brain, astrocytes provide crucial support to neurons and participate in synapse formation, synaptic transmission, neurotransmitter recycling, regulation of metabolic processes, and the maintenance of the blood-brain barrier integrity. Though astrocytes play a significant role in the manifestation of injury and disease, they do not work in isolation. Cellular interactions between astrocytes and neurons are essential for maintaining the homeostasis of the CNS under both physiological and pathological conditions. In this review, we explore the diverse interactions between astrocytes and neurons under physiological conditions, including the exchange of neurotrophic factors, gliotransmitters, and energy substrates, and different CNS diseases such as Alzheimer’s disease, Parkinson’s disease, stroke, traumatic brain injury, and multiple sclerosis. This review sheds light on the contribution of astrocyte-neuron crosstalk to the progression of neurological diseases to provide potential therapeutic targets for the treatment of neurological diseases.

神经元是中枢神经系统(CNS)中负责信息处理的主要细胞。然而,在各种神经系统疾病中,神经元很容易受到损害和损伤。作为大脑中最丰富的胶质细胞,星形胶质细胞为神经元提供重要支持,并参与突触形成、突触传递、神经递质循环、代谢过程调节和血脑屏障完整性的维护。虽然星形胶质细胞在损伤和疾病的表现中起着重要作用,但它们并不是孤立地工作的。在生理和病理条件下,星形胶质细胞和神经元之间的细胞相互作用对于维持中枢神经系统的平衡至关重要。在这篇综述中,我们探讨了星形胶质细胞和神经元在生理条件下的各种相互作用,包括神经营养因子、胶质递质和能量底物的交换,以及阿尔茨海默病、帕金森病、中风、脑外伤和多发性硬化症等不同中枢神经系统疾病。这篇综述揭示了星形胶质细胞-神经元串扰对神经系统疾病进展的影响,为治疗神经系统疾病提供了潜在的治疗靶点。
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引用次数: 0
Correction: Nuclear Medicine Imaging Techniques in Glioblastomas 更正:胶质母细胞瘤的核医学成像技术。
IF 3.7 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-18 DOI: 10.1007/s11064-024-04247-0
Emirhan Harbi, Michael Aschner
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引用次数: 0
期刊
Neurochemical Research
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