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Abel Lajtha: In Memoriam (1922–2024) 阿贝尔-拉伊萨悼念(1922-2024 年)。
IF 3.7 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-18 DOI: 10.1007/s11064-024-04187-9
Henry Sershen
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引用次数: 0
The Protective Role of Transcript-Induced in Spermiogenesis 40 in Cerebral Ischemia–Reperfusion Injury 转录本诱导的精子生成40在脑缺血再灌注损伤中的保护作用
IF 3.7 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-17 DOI: 10.1007/s11064-024-04170-4
Jing Xie, Lei Wang, Song Tian, Ruyan Li, Li Zhang, Hongjie Shi, Zhen Liu, Tengfei Ma, Heng Hu, Zhigang She, Lang wang

Prompt reperfusion after cerebral ischemia is important to maintain neuronal survival and reduce permanent disability and death. However, the resupply of blood can induce oxidative stress, inflammatory response and apoptosis, further leading to tissue damage. Here, we report the versatile biological roles of transcript-induced in spermiogenesis 40 (Tisp40) in ischemic stroke. We found that the expression of Tisp40 was upregulated in ischemia/reperfusion-induced brain tissues and oxygen glucose deprivation/returned -stimulated neurons. Tisp40 deficiency increased the infarct size and neurological deficit score, and promoted inflammation and apoptosis. Tisp40 overexpression played the opposite role. In vitro, the oxygen glucose deprivation/returned model was established in Tisp40 knockdown and overexpression primary cultured cortical neurons. Tisp40 knockdown can aggravate the process of inflammation and apoptosis, and Tisp40 overexpression ameliorated the aforementioned processes. Mechanistically, Tisp40 protected against ischemic stroke via activating the AKT signaling pathway. Tisp40 may be a new therapeutic target in brain ischemia/reperfusion injury.

脑缺血后及时再灌注对于维持神经元存活、减少永久性残疾和死亡非常重要。然而,血液补给会诱发氧化应激、炎症反应和细胞凋亡,进一步导致组织损伤。在此,我们报告了转录本诱导的精子发生40(Tisp40)在缺血性中风中的多种生物学作用。我们发现,Tisp40在缺血/再灌注诱导的脑组织和氧糖剥夺/回流刺激的神经元中表达上调。Tisp40 缺乏会增加梗死面积和神经功能缺损评分,并促进炎症和细胞凋亡。Tisp40过表达则起相反的作用。在体外,Tisp40敲除和过表达原代培养的皮层神经元建立了氧糖剥夺/回流模型。Tisp40敲除可加重炎症和细胞凋亡过程,而Tisp40过表达则可改善上述过程。从机理上讲,Tisp40通过激活AKT信号通路保护缺血性中风。Tisp40可能是脑缺血再灌注损伤的一个新的治疗靶点。
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引用次数: 0
Glioprotective Effects of Sulforaphane in Hypothalamus: Focus on Aging Brain 下丘脑中的神经胶质保护作用:聚焦老化大脑
IF 3.7 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-17 DOI: 10.1007/s11064-024-04196-8
Camila Leite Santos, Fernanda Becker Weber, Adriane Belló-Klein, Larissa Daniele Bobermin, André Quincozes-Santos

Sulforaphane is a natural compound with neuroprotective activity, but its effects on hypothalamus remain unknown. In line with this, astrocytes are critical cells to maintain brain homeostasis, and hypothalamic astrocytes are fundamental for sensing and responding to environmental changes involved in a variety of homeostatic functions. Changes in brain functionality, particularly associated with hypothalamic astrocytes, can contribute to age-related neurochemical alterations and, consequently, neurodegenerative diseases. Thus, here, we investigated the glioprotective effects of sulforaphane on hypothalamic astrocyte cultures and hypothalamic cell suspension obtained from aged Wistar rats (24 months old). Sulforaphane showed anti-inflammatory and antioxidant properties, as well as modulated the mRNA expression of astroglial markers, such as aldehyde dehydrogenase 1 family member L1, aquaporin 4, and vascular endothelial growth factor. In addition, it increased the expression and extracellular levels of trophic factors, such as glia-derived neurotrophic factor and nerve growth factor, as well as the release of brain-derived neurotrophic factor and the mRNA of TrkA, which is a receptor associated with trophic factors. Sulforaphane also modulated the expression of classical pathways associated with glioprotection, including nuclear factor erythroid-derived 2-like 2, heme oxygenase-1, nuclear factor kappa B p65 subunit, and AMP-activated protein kinase. Finally, a cell suspension with neurons and glial cells was used to confirm the predominant effect of sulforaphane in glial cells. In summary, this study indicated the anti-aging and glioprotective activities of sulforaphane in aged astrocytes.

红豆杉是一种具有神经保护活性的天然化合物,但其对下丘脑的影响尚不清楚。因此,星形胶质细胞是维持大脑平衡的关键细胞,而下丘脑星形胶质细胞是感知和响应环境变化的基本细胞,参与多种平衡功能。大脑功能的变化,尤其是与下丘脑星形胶质细胞相关的变化,可能会导致与年龄相关的神经化学改变,进而引发神经退行性疾病。因此,我们在此研究了莱菔硫烷对下丘脑星形胶质细胞培养物和下丘脑细胞悬浮液的神经胶质保护作用,这些培养物和细胞悬浮液均取自年老的 Wistar 大鼠(24 个月大)。莱菔硫烷具有抗炎和抗氧化特性,并能调节星形胶质细胞标志物(如醛脱氢酶 1 家族成员 L1、水光素 4 和血管内皮生长因子)的 mRNA 表达。此外,它还能增加神经胶质细胞生长因子和神经生长因子等营养因子的表达和细胞外水平,以及脑源性神经营养因子和与营养因子相关的受体 TrkA 的 mRNA 的释放。红景天还能调节与胶质保护相关的经典通路的表达,包括核因子红细胞衍生 2-like 2、血红素加氧酶-1、核因子卡巴 B p65 亚基和 AMP 激活蛋白激酶。最后,研究人员利用神经元和神经胶质细胞的细胞悬浮液证实了红景天对神经胶质细胞的主要作用。总之,这项研究表明了莱菔硫烷在老年星形胶质细胞中的抗衰老和胶质保护活性。
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引用次数: 0
The Role of Ferroptosis in Amyotrophic Lateral Sclerosis Treatment 铁蛋白沉积在肌萎缩侧索硬化症治疗中的作用
IF 3.7 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-12 DOI: 10.1007/s11064-024-04194-w
Le Yi Wang, Lei Zhang, Xin Yue Bai, Rong Rong Qiang, Ning Zhang, Qian Qian Hu, Jun Zhi Cheng, Yan Ling Yang, Yang Xiang

Amyotrophic lateral sclerosis (ALS) is a rare neurodegenerative disease with a challenging treatment landscape, due to its complex pathogenesis and limited availability of clinical drugs. Ferroptosis, an iron-dependent form of programmed cell death (PCD), stands distinct from apoptosis, necrosis, autophagy, and other cell death mechanisms. Recent studies have increasingly highlighted the role of iron deposition, reactive oxygen species (ROS) accumulation, oxidative stress, as well as systemic Xc- and glutamate accumulation in the antioxidant system in the pathogenesis of amyotrophic lateral sclerosis. Therefore, targeting ferroptosis emerges as a promising strategy for amyotrophic lateral sclerosis treatment. This review introduces the regulatory mechanism of ferroptosis, the relationship between amyotrophic lateral sclerosis and ferroptosis, and the drugs used in the clinic, then discusses the current status of amyotrophic lateral sclerosis treatment, hoping to provide new directions and targets for its treatment.

肌萎缩性脊髓侧索硬化症(ALS)是一种罕见的神经退行性疾病,由于其发病机制复杂,临床药物有限,因此治疗前景充满挑战。铁凋亡是细胞程序性死亡(PCD)的一种铁依赖形式,有别于细胞凋亡、坏死、自噬和其他细胞死亡机制。最近的研究越来越多地强调了铁沉积、活性氧(ROS)积累、氧化应激以及抗氧化系统中系统性 Xc 和谷氨酸积累在肌萎缩侧索硬化症发病机制中的作用。因此,靶向铁蛋白沉积是治疗肌萎缩性侧索硬化症的一种有前景的策略。本综述介绍了铁变态反应的调控机制、肌萎缩性脊髓侧索硬化症与铁变态反应的关系以及临床应用的药物,并探讨了肌萎缩性脊髓侧索硬化症的治疗现状,希望能为肌萎缩性脊髓侧索硬化症的治疗提供新的方向和靶点。
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引用次数: 0
Neuroprotective Action of Selected Natural Drugs Against Neurological Diseases and Mental Disorders: Potential Use Against Radiation Damage 某些天然药物对神经系统疾病和精神障碍的神经保护作用:对抗辐射损伤的潜在用途。
IF 3.7 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-12 DOI: 10.1007/s11064-024-04184-y
Akhlada, Nazia Siddiqui,  Anurag, Alimuddin Saifi, Anuradha Kesharwani, Vipan Kumar Parihar, Alok Sharma

Exposure to radiation, ionizing and non-ionizing radiation, is a significant concern in modern society. The brain is the organ that is most sensitive to radiation exposure. This review describes how exposure to radiation can affect neurotransmitters in different brain regions, affecting brain function. This review covers neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and neuroinflammation due to changes in neurons in the central nervous system, and the effects thereon of medicinal plants such as Allium cepa, Allium sativum, Centella asiatica, Coriandrum sativum, and Crocus sativus plants, used for centuries in traditional medicine. These herbal medicines exert free radical scavenging, and antioxidant as well as anti-inflammatory properties which can be beneficial in managing neurological diseases. The present review compiles the neuroprotective effects of selected natural plants against neurological damage, as well as highlights the different mechanisms of action elicited to induce and produce beneficial effects. The current review describes recent studies on the pharmacological effects of neuroprotective herbs on various neurological and mental illnesses, and shows the way further studies can impact this field, including potential effects on radiation-induced damage.

现代社会对辐射、电离辐射和非电离辐射的关注度很高。大脑是对辐射最敏感的器官。本综述介绍了辐照如何影响不同脑区的神经递质,从而影响大脑功能。本综述涉及阿尔茨海默氏症、帕金森氏症等神经退行性疾病和中枢神经系统神经元变化引起的神经炎症,以及在传统医学中使用了几个世纪的薤白、薤白、积雪草、芫荽和茜草等药用植物对这些疾病的影响。这些草药具有清除自由基、抗氧化和抗炎的特性,可用于治疗神经系统疾病。本综述汇编了部分天然植物对神经损伤的神经保护作用,并重点介绍了诱导和产生有益作用的不同作用机制。本综述介绍了近期关于神经保护草药对各种神经和精神疾病的药理作用的研究,并展示了进一步研究对这一领域的影响,包括对辐射引起的损伤的潜在影响。
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引用次数: 0
Both Enantiomers of 2-Hydroxyglutarate Modulate the Metabolism of Cultured Human Neuroblastoma Cells 2-羟基戊二酸的两种对映体都能调节培养的人神经母细胞瘤细胞的新陈代谢
IF 3.7 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-12 DOI: 10.1007/s11064-024-04188-8
Eduard Gondáš, Eva Baranovičová, Peter Bystrický, Jakub Šofranko, Andrea Evinová, Matúš Dohál, Zuzana Hatoková, Radovan Murín

Elevated levels of D-2-hydroxyglutarate (D-2HG) and L-2-hydroxyglutarate (L-2HG) in the brain are associated with various pathological conditions, potentially contributing to neurological symptoms and neurodegeneration. Previous studies on animal models have revealed their capability to interfere with several cellular processes, including mitochondrial metabolism. Both enantiomers competitively inhibit the enzymatic activity of 2-oxoglutarate-dependent dioxygenases. These enzymes also execute several signaling cascades and regulate the level of covalent modifications on nucleic acids or proteins, e.g., methylation, hydroxylation, or ubiquitination, with an effect on epigenetic regulation of gene expression, protein stability, and intracellular signaling. To investigate the potential impact of 2HG enantiomers on human neuronal cells, we utilized the SH-SY5Y human neuroblastoma cell line as a model. We employed proton nuclear magnetic resonance (1H-NMR) spectroscopy of culture media that provided high-resolution insights into the changes in the content of metabolites. Concurrently, we performed biochemical assays to complement the 1H-NMR findings and to estimate the activities of lactate and 3-hydroxybutyrate dehydrogenases. Our results reveal that both 2HG enantiomers can influence the cellular metabolism of human neuroblastoma cells on multiple levels. Specifically, both enantiomers of 2HG comparably stimulate anaerobic metabolism of glucose and inhibit the uptake of several essential amino acids from the culture media. In this respect, both 2HG enantiomers decreased the catabolism capability of cells to incorporate the leucine-derived carbon atoms into their metabolism and to generate the ketone bodies. These results provide evidence that both enantiomers of 2HG have the potential to influence the metabolic and molecular aspects of human cells. Furthermore, we may propose that increased levels of 2HG enantiomers in the brain parenchyma may alter brain metabolism features, potentially contributing to the etiology of neurological symptoms in patients.

大脑中 D-2-羟基戊二酸(D-2HG)和 L-2-羟基戊二酸(L-2HG)水平的升高与各种病理情况有关,可能会导致神经症状和神经变性。以前对动物模型的研究表明,它们能够干扰多种细胞过程,包括线粒体代谢。这两种对映体都能竞争性地抑制依赖 2-氧代戊二酸的二氧酶的酶活性。这些酶还执行多个信号级联,并调节核酸或蛋白质的共价修饰水平,如甲基化、羟基化或泛素化,从而影响基因表达的表观遗传调控、蛋白质稳定性和细胞内信号转导。为了研究 2HG 对映异构体对人类神经细胞的潜在影响,我们以 SH-SY5Y 人类神经母细胞瘤细胞系为模型。我们采用质子核磁共振(1H-NMR)光谱对培养基进行分析,从而高分辨率地了解代谢物含量的变化。与此同时,我们还进行了生化测定,以补充 1H-NMR 研究结果,并估算乳酸脱氢酶和 3- 羟基丁酸脱氢酶的活性。我们的研究结果表明,两种 2HG 对映异构体都能在多个层面上影响人神经母细胞瘤细胞的新陈代谢。具体来说,2HG 的两种对映体都能刺激葡萄糖的无氧代谢,并抑制培养基中几种必需氨基酸的吸收。在这方面,两种 2HG 对映异构体都降低了细胞将亮氨酸衍生碳原子纳入其代谢和生成酮体的分解能力。这些结果证明,2HG 的两种对映体都有可能影响人体细胞的代谢和分子方面。此外,我们还可以认为,脑实质中 2HG 对映异构体含量的增加可能会改变脑代谢特征,从而有可能导致患者出现神经系统症状。
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引用次数: 0
Idebenone Antagonizes P53-Mediated Neuronal Oxidative Stress Injury by Regulating CD38-SIRT3 Protein Level 艾地苯醌通过调节CD38-SIRT3蛋白水平拮抗P53介导的神经元氧化应激损伤
IF 3.7 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-12 DOI: 10.1007/s11064-024-04189-7
Hao Xu, Ying Guo, Xiao-Jun Liu, Ying Liu, Shi Yin, Qi-Ying Bao, Ru Peng, Wei-Bo Tian, Ying-Yan Xia, Ling Gao, Jia-Mei Liu

Idebenone, an antioxidant used in treating oxidative damage-related diseases, has unclear neuroprotective mechanisms. Oxidative stress affects cell and mitochondrial membranes, altering Adp-ribosyl cyclase (CD38) and Silent message regulator 3 (SIRT3) protein expression and possibly impacting SIRT3’s ability to deacetylate Tumor protein p53 (P53). This study explores the relationship between CD38, SIRT3, and P53 in H2O2-injured HT22 cells treated with Idebenone. Apoptosis was detected using flow cytometry and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining after determining appropriate H2O2 and Idebenone concentrations.

In this study, Idebenone was found to reduce apoptosis and decrease P53 and Caspase3 expression in H2O2-injured HT22 cells by detecting apoptosis-related protein expression. Through bioinformatics methods, CD38 was identified as the target of Idebenone, and it further demonstrated that Idebenone decreased the expression of CD38 and increased the level of SIRT3. An increased NAD+/NADH ratio was detected, suggesting Idebenone induces SIRT3 expression and protects HT22 cells by decreasing apoptosis-related proteins. Knocking down SIRT3 downregulated acetylated P53 (P53Ac), indicating SIRT3’s importance in P53 deacetylation.

These results supported that CD38 was used as a target of Idebenone to up-regulate SIRT3 to deacetylate activated P53, thereby protecting HT22 cells from oxidative stress injury. Thus, Idebenone is a drug that may show great potential in protecting against reactive oxygen species (ROS) induced diseases such as Parkinson’s disease, and Alzheimer’s disease. And it might be able to compensate for some of the defects associated with CD38-related diseases.

艾地苯醌是一种用于治疗氧化损伤相关疾病的抗氧化剂,其神经保护机制尚不清楚。氧化应激会影响细胞膜和线粒体膜,改变 Adp 核糖环化酶(CD38)和沉默信息调节因子 3(SIRT3)蛋白的表达,并可能影响 SIRT3 对肿瘤蛋白 p53(P53)的去乙酰化能力。本研究探讨了伊地苯醌处理的 H2O2 损伤 HT22 细胞中 CD38、SIRT3 和 P53 之间的关系。本研究通过检测细胞凋亡相关蛋白的表达,发现艾地苯醌可减少H2O2损伤的HT22细胞的细胞凋亡,并降低P53和Caspase3的表达。通过生物信息学方法,CD38被确定为艾地苯醌的靶点,并进一步证明艾地苯醌能降低CD38的表达,提高SIRT3的水平。检测到NAD+/NADH比值升高,表明艾地苯酮能诱导SIRT3的表达,并通过减少凋亡相关蛋白来保护HT22细胞。敲除 SIRT3 会降低乙酰化 P53 (P53Ac),表明 SIRT3 在 P53 去乙酰化过程中的重要性。这些结果证明,CD38 可作为艾地苯醌的靶点,上调 SIRT3 使活化的 P53 去乙酰化,从而保护 HT22 细胞免受氧化应激损伤。因此,艾地苯醌是一种在保护帕金森病和阿尔茨海默病等由活性氧(ROS)诱发的疾病方面具有巨大潜力的药物。而且,它还可能弥补 CD38 相关疾病的一些缺陷。
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引用次数: 0
Epigenetic Orchestration of Neurodegenerative Disorders: A Possible Target for Curcumin as a Therapeutic 神经退行性疾病的表观遗传协调:姜黄素作为治疗剂的一个可能靶点
IF 3.7 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-10 DOI: 10.1007/s11064-024-04167-z
Shweta Tripathi,  Bhawana

Epigenetic modulations play a major role in gene expression and thus are responsible for various physiological changes including age-associated neurological disorders. Neurodegenerative diseases such as Alzheimer’s (AD), Parkinson’s (PD), Huntington’s disease (HD), although symptomatically different, may share common underlying mechanisms. Most neurodegenerative diseases are associated with increased oxidative stress, aggregation of certain proteins, mitochondrial dysfunction, inactivation/dysregulation of protein degradation machinery, DNA damage and cell excitotoxicity. Epigenetic modulations has been reported to play a significant role in onset and progression of neurodegenerative diseases by regulating these processes. Previous studies have highlighted the marked antioxidant and neuroprotective abilities of polyphenols such as curcumin, by increased activity of detoxification systems like superoxide dismutase (SOD), catalase or glutathione peroxidase. The role of curcumin as an epigenetic modulator in neurological disorders and neuroinflammation apart from other chronic diseases have also been reported by a few groups. Nonetheless, the evidences for the role of curcumin mediated epigenetic modulation in its neuroprotective ability are still limited. This review summarizes the current knowledge of the role of mitochondrial dysfunction, epigenetic modulations and mitoepigenetics in age-associated neurological disorders such as PD, AD, HD, Amyotrophic Lateral Sclerosis (ALS), and Multiple Sclerosis (MS), and describes the neuroprotective effects of curcumin in the treatment and/or prevention of these neurodegenerative diseases by regulation of the epigenetic machinery.

表观遗传调控在基因表达中起着重要作用,因此是导致各种生理变化(包括与年龄相关的神经系统疾病)的原因。阿尔茨海默病(AD)、帕金森病(PD)、亨廷顿病(HD)等神经退行性疾病虽然症状不同,但可能具有共同的潜在机制。大多数神经退行性疾病都与氧化应激增加、某些蛋白质聚集、线粒体功能障碍、蛋白质降解机制失活/失调、DNA 损伤和细胞兴奋毒性有关。据报道,表观遗传调节通过调节这些过程,在神经退行性疾病的发生和发展中发挥着重要作用。以往的研究强调,姜黄素等多酚类物质通过提高超氧化物歧化酶(SOD)、过氧化氢酶或谷胱甘肽过氧化物酶等解毒系统的活性,具有明显的抗氧化和神经保护能力。一些研究小组还报告了姜黄素作为表观遗传调节剂在神经系统疾病和神经炎症以及其他慢性疾病中的作用。然而,姜黄素介导的表观遗传调节在其神经保护能力中所起作用的证据仍然有限。本综述总结了线粒体功能障碍、表观遗传调控和线粒体表观遗传学在与年龄相关的神经系统疾病(如帕金森病、多发性硬化症、肌萎缩侧索硬化症和多发性硬化症)中的作用,并介绍了姜黄素通过调控表观遗传机制在治疗和/或预防这些神经退行性疾病中的神经保护作用。
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引用次数: 0
Role of Brain Derived Neurotrophic Factor and Related Therapeutic Strategies in Central Post-Stroke Pain 脑源性神经营养因子在中枢性卒中后疼痛中的作用及相关治疗策略
IF 3.7 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-10 DOI: 10.1007/s11064-024-04175-z
Gayathri Rajamanickam, Andy Thiam Huat Lee, Ping Liao

Brain-derived neurotrophic factor (BDNF) is vital for synaptic plasticity, cell persistence, and neuronal development in peripheral and central nervous systems (CNS). Numerous intracellular signalling pathways involving BDNF are well recognized to affect neurogenesis, synaptic function, cell viability, and cognitive function, which in turn affects pathological and physiological aspects of neurons. Stroke has a significant psycho-socioeconomic impact globally. Central post-stroke pain (CPSP), also known as a type of chronic neuropathic pain, is caused by injury to the CNS following a stroke, specifically damage to the somatosensory system. BDNF regulates a broad range of functions directly or via its biologically active isoforms, regulating multiple signalling pathways through interactions with different types of receptors. BDNF has been shown to play a major role in facilitating neuroplasticity during post-stroke recovery and a pro-nociceptive role in pain development in the nervous system. BDNF-tyrosine kinase receptors B (TrkB) pathway promotes neurite outgrowth, neurogenesis, and the prevention of apoptosis, which helps in stroke recovery. Meanwhile, BDNF overexpression plays a role in CPSP via the activation of purinergic receptors P2X4R and P2X7R. The neuronal hyperexcitability that causes CPSP is linked with BDNF-TrkB interactions, changes in ion channels and inflammatory reactions. This review provides an overview of BDNF synthesis, interactions with certain receptors, and potential functions in regulating signalling pathways associated with stroke and CPSP. The pathophysiological mechanisms underlying CPSP, the role of BDNF in CPSP, and the challenges and current treatment strategies targeting BDNF are also discussed.

脑源性神经营养因子(BDNF)对周围和中枢神经系统(CNS)的突触可塑性、细胞持久性和神经元发育至关重要。涉及 BDNF 的众多细胞内信号通路被公认会影响神经发生、突触功能、细胞活力和认知功能,进而影响神经元的病理和生理方面。脑卒中对全球的社会心理经济产生了重大影响。中风后中枢疼痛(CPSP)也被称为一种慢性神经病理性疼痛,是中风后中枢神经系统损伤,特别是躯体感觉系统损伤引起的。BDNF 可直接或通过其生物活性异构体调节多种功能,通过与不同类型受体的相互作用调节多种信号通路。研究表明,BDNF 在促进中风后恢复过程中的神经可塑性方面发挥着重要作用,并在神经系统的疼痛发展过程中发挥着促进痛觉的作用。BDNF-酪氨酸激酶受体 B(TrkB)通路可促进神经元突起、神经发生和防止细胞凋亡,有助于脑卒中的恢复。同时,BDNF 过表达通过激活嘌呤能受体 P2X4R 和 P2X7R 在 CPSP 中发挥作用。导致 CPSP 的神经元过度兴奋与 BDNF-TrkB 相互作用、离子通道变化和炎症反应有关。本综述概述了 BDNF 的合成、与某些受体的相互作用以及在调节与中风和 CPSP 相关的信号通路方面的潜在功能。此外,还讨论了 CPSP 的病理生理机制、BDNF 在 CPSP 中的作用以及针对 BDNF 的挑战和当前治疗策略。
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引用次数: 0
Types of Short-Duration Electrical Stimulation-Induced Efficiency in the Axonal Regeneration and Recovery: Comparative in Vivo Study in Rat Model of Repaired Sciatic Nerve and its Tibial Branch after Transection Injury 短时电刺激在轴突再生和恢复中的效率类型:大鼠坐骨神经及其胫骨支切断损伤后修复模型的体内比较研究。
IF 3.7 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-10 DOI: 10.1007/s11064-024-04154-4
Sareh Naseri, Hosein Samaram, Nadia Naghavi, Morteza Behnam Rassouli, Maryam Mousavinezhad

The restoration of adequate function and sensation in nerves following an injury is often insufficient. Electrical stimulation (ES) applied during nerve repair can promote axon regeneration, which may enhance the likelihood of successful functional recovery. However, increasing operation time and complexity are associated with limited clinical use of ES. This study aims to better assess whether short-duration ES types (voltage mode vs. current mode) are able to produce enhanced regenerative activity following peripheral nerve repair in rat models. Wistar rats were randomly divided into 3 groups: no ES (control), 30-minute ES with a current pulse, and 30-minute ES with a voltage pulse. All groups underwent sciatic nerve transection and repair using a silicone tube to bridge the 6-mm gap between the stumps. In the 2 groups other than the control, ES was applied after the surgical repair. Outcomes were evaluated using electrophysiology, histology, and serial walking track analysis. Biweekly walking tracks test over 12 weeks revealed that subjects that underwent ES experienced more rapid functional improvement than subjects that underwent repair alone. Electrophysiological analysis of the newly intratubular sciatic nerve at week 12 revealed strong motor function recovery in rats that underwent 30-minute ES. Histologic analysis of the sciatic nerve and its tibial branch at 12 weeks demonstrated robust axon regrowth in all groups. Both types of short-duration ES applied during nerve repair can promote axon regrowth and enhance the chances of successful functional recovery.

神经受伤后,其功能和感觉往往无法充分恢复。在神经修复过程中应用电刺激(ES)可促进轴突再生,从而提高功能成功恢复的可能性。然而,随着手术时间和复杂程度的增加,ES 的临床应用受到限制。本研究旨在更好地评估短时ES类型(电压模式与电流模式)是否能在大鼠模型的周围神经修复后产生更强的再生活性。Wistar 大鼠被随机分为 3 组:无 ES 组(对照组)、30 分钟电流脉冲 ES 组和 30 分钟电压脉冲 ES 组。所有组都进行了坐骨神经横断和修复,使用硅胶管弥合残端之间 6 毫米的间隙。除对照组外的两组在手术修复后使用 ES。结果通过电生理学、组织学和连续行走轨迹分析进行评估。为期 12 周的双周步行轨迹测试显示,接受 ES 治疗的受试者比单纯接受修复治疗的受试者的功能改善更快。在第 12 周对新插入的坐骨神经进行的电生理分析显示,接受 30 分钟 ES 治疗的大鼠的运动功能得到了很好的恢复。在 12 周时对坐骨神经及其胫骨分支进行的组织学分析表明,所有组别都有强劲的轴突再生。在神经修复过程中应用这两种短时 ES 都能促进轴突再生,提高功能成功恢复的几率。
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Neurochemical Research
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