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Honouring Geoff Burnstock. 向杰夫-伯恩斯托克致敬
IF 3 4区 医学 Q2 NEUROSCIENCES Pub Date : 2024-11-05 DOI: 10.1007/s11302-024-10061-8
Yong Tang, Peter Illes, Charles Kennedy
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引用次数: 0
The exploration of active components of 701 Dieda Zhentong patch and analgesic properties on chronic constriction injury rats. 701地达镇痛贴有效成分及对慢性收缩性损伤大鼠镇痛作用的探讨
IF 3 4区 医学 Q2 NEUROSCIENCES Pub Date : 2024-11-04 DOI: 10.1007/s11302-024-10056-5
Jun Meng, Zhenglang Zhang, Yujie Wang, Lina Long, Anqi Luo, Zhenhui Luo, Kexin Cai, Xi Chen, Hong Nie

An increasing number of traditional Chinese medicine(TCM) have been confirmed to possess analgesic bioactivity. 701 Dieda Zhentong patch(701-DZP) which includes 14 kinds of TCMs exhibited excellent efficacy in alleviating back or leg pain after a soft-tissue injury. In this study, UPLC/MS was used to construct the fingerprint of 701-DZP and excavate the potential bioactive ingredients of it. 21 compounds were detected and identified in the fingerprint including 12 compounds that pass through the skin and 6 compounds observed in the plasma. Then, the role of 701-DZP in neuropathic pain(NPP) was assessed by network pharmacology and CCI rats. 701-DZP inhibited pain sensitization(MWT and TWL) and the release of inflammation mediators(IL-1β and IL-6) in CCI rats which were in keeping with the core targets of the PPI network. The results of IHC and Western blot showed that the expression of the P2X3 receptor in the DRG and SC of CCI rats was significantly reduced after the treatment with 701-DZP. Moreover, the 701-DZP down-regulated the level of phosphorylation of ERK1/2 MAPK instead of P38 MAPK in the DRG of CCI rats. In conclusion, this study has clarified 6 potential analgesic active compounds of 701-DZP and explored the analgesic properties, which may inhibit the expression of the P2X3 receptor to reduce the release of inflammatory mediators based on the ERK1/2 MAPK pathway to alleviate the NPP.

越来越多的传统中药被证实具有镇痛生物活性。由 14 种中药组成的 701 Dieda Zhentong 贴片(701-DZP)在缓解软组织损伤后的腰腿痛方面表现出卓越的疗效。本研究采用UPLC/MS构建了701-DZP的指纹图谱,并挖掘了其中潜在的生物活性成分。在指纹图谱中检测并确定了 21 种化合物,包括 12 种通过皮肤的化合物和 6 种在血浆中观察到的化合物。然后,通过网络药理学和 CCI 大鼠评估了 701-DZP 在神经病理性疼痛(NPP)中的作用。701-DZP抑制了CCI大鼠的痛敏化(MWT和TWL)和炎症介质(IL-1β和IL-6)的释放,这与PPI网络的核心目标一致。IHC和Western blot结果显示,701-DZP治疗后,CCI大鼠DRG和SC中P2X3受体的表达明显减少。此外,701-DZP还能下调CCI大鼠DRG中ERK1/2 MAPK而非P38 MAPK的磷酸化水平。总之,本研究阐明了 701-DZP 的 6 种潜在镇痛活性化合物,并探讨了其镇痛特性,这些化合物可能会抑制 P2X3 受体的表达,从而减少基于 ERK1/2 MAPK 通路的炎症介质的释放,从而缓解 NPP。
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引用次数: 0
Role of adenosine in the pathophysiology and treatment of attention deficit hyperactivity disorder. 腺苷在注意缺陷多动障碍的病理生理学和治疗中的作用。
IF 3 4区 医学 Q2 NEUROSCIENCES Pub Date : 2024-10-31 DOI: 10.1007/s11302-024-10059-2
Qingxia Jia, Hongwan Tan, Tingsong Li, Xiaoling Duan

Attention deficit hyperactivity disorder (ADHD) is a complex neurodevelopmental condition characterized by persistent inattention, hyperactivity, and impulsivity. Although its precise etiology remains unclear, current evidence suggests that dysregulation within the neurotransmitter system plays a key role in the pathogenesis of ADHD. Adenosine, an endogenous nucleoside widely distributed throughout the body, modulates various physiological processes, including neurotransmitter release, sleep regulation, and cognitive functions through its receptors. This review critically examines the role of the adenosine system in ADHD, focusing on the links between adenosine receptor function and ADHD-related symptoms. Additionally, it explores how adenosine interacts with dopamine and other neurotransmitter pathways, shedding light on its involvement in ADHD pathophysiology. This review aims to provide insights into the potential therapeutic implications of targeting the adenosine system for ADHD management.

注意缺陷多动障碍(ADHD)是一种复杂的神经发育疾病,其特征是持续的注意力不集中、多动和冲动。虽然其确切的病因尚不清楚,但目前的证据表明,神经递质系统失调在多动症的发病机制中起着关键作用。腺苷是一种广泛分布于人体各处的内源性核苷,可通过其受体调节各种生理过程,包括神经递质释放、睡眠调节和认知功能。本综述批判性地研究了腺苷系统在多动症中的作用,重点关注腺苷受体功能与多动症相关症状之间的联系。此外,它还探讨了腺苷如何与多巴胺和其他神经递质通路相互作用,从而揭示腺苷在多动症病理生理学中的作用。本综述旨在深入探讨针对腺苷系统治疗多动症的潜在治疗意义。
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引用次数: 0
P2Y12 receptor-mediated cyclooxygenase 2 (COX-2) expression enhances tumor cell progression in a mouse model of lymphoma. 在小鼠淋巴瘤模型中,P2Y12 受体介导的环氧化酶 2 (COX-2) 表达可促进肿瘤细胞的发展。
IF 3 4区 医学 Q2 NEUROSCIENCES Pub Date : 2024-10-29 DOI: 10.1007/s11302-024-10057-4
Shilpa Sharma, Khagendra Ghimeray, Md Mostafizur Rahman, Aparna Upadrasta, Ravi Shankar Akundi

The pro-inflammatory enzyme cyclooxygenase 2 (COX-2) has been known to impart metastatic property to cancer cells. However, blocking of COX-2 with nonsteroidal anti-inflammatory drugs or COX-2-specific inhibitors has failed in clinical trials due to adverse effects associated with their prolonged use. We have previously shown that extracellular ATP (eATP), a major component of the tumor microenvironment, enhances COX-2 expression several-fold, both in macrophages and in various cancer cells, by acting on purinergic (P2) receptors. In this study, we show that blocking of P2 receptors significantly reduced tumor growth in a mouse model of lymphoma. Tumors were induced in mice through subcutaneous injection of syngeneic EL4 lymphoma cells. Various P2 receptor antagonists were injected within the tumors after they were palpable. The broad-spectrum P2 receptor antagonist, suramin, P2X7 receptor-specific antagonist, oATP, P2Y6 receptor-specific antagonist, MRS 2578, and P2Y12 receptor-specific antagonist, AR-C 69931, all showed significant arrest in tumor growth. Both suramin and AR-C 69931-treated tumors showed strong reduction in COX-2 expression and modulation of various metastatic markers. Disaggregated cells from AR-C 69931-treated tumors, when injected intravenously in naïve mice, did not exhibit metastasis in various tissues which was observed in mice injected with cells from saline-treated tumors. Our results show that blocking of P2 receptors is a therapeutic alternative to inhibit COX-2 expression, and thereby, arrest tumor progression and metastasis.

众所周知,促炎酶环氧化酶 2(COX-2)可赋予癌细胞转移特性。然而,用非甾体抗炎药或 COX-2 特异性抑制剂阻断 COX-2,在临床试验中却以失败告终,原因是长期使用会产生不良反应。我们以前的研究表明,细胞外 ATP(eATP)是肿瘤微环境的主要成分,它通过作用于嘌呤能(P2)受体,使巨噬细胞和各种癌细胞中 COX-2 的表达增强数倍。本研究表明,在小鼠淋巴瘤模型中,阻断 P2 受体可显著减少肿瘤生长。小鼠通过皮下注射合成 EL4 淋巴瘤细胞诱发肿瘤。在摸到肿瘤后,在肿瘤内注射各种 P2 受体拮抗剂。广谱 P2 受体拮抗剂舒拉明、P2X7 受体特异性拮抗剂 oATP、P2Y6 受体特异性拮抗剂 MRS 2578 和 P2Y12 受体特异性拮抗剂 AR-C 69931 都能显著抑制肿瘤生长。苏拉明和 AR-C 69931 处理过的肿瘤都显示 COX-2 的表达明显减少,各种转移标记物的表达也有所改变。将 AR-C 69931 处理过的肿瘤分解细胞静脉注射给天真小鼠后,小鼠在各种组织中均未出现转移,而注射生理盐水处理过的肿瘤细胞的小鼠则出现了这种情况。我们的研究结果表明,阻断 P2 受体是抑制 COX-2 表达从而阻止肿瘤进展和转移的一种治疗方法。
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引用次数: 0
Screening herbal and natural product libraries to aid discovery of novel allosteric modulators of human P2X7. 筛选草药和天然产品库,帮助发现新型人类 P2X7 异构调节剂。
IF 3 4区 医学 Q2 NEUROSCIENCES Pub Date : 2024-10-22 DOI: 10.1007/s11302-024-10055-6
Stefan Bidula, Waraporn Piyasirananda, Hanna Bielecka, Lučka Bibič, Andrew Beekman, Leanne Stokes

 P2X7 is an emerging therapeutic target for several disorders and diseases due to its role in inflammatory signalling. This study aimed to exploit the unique chemical libraries of plants used in traditional medicinal practices to discover novel allosteric modulators from natural sources. We identified several compounds from the NCI Natural Product library as P2X7 antagonists including confertifolin and digallic acid (IC50 values 3.86 µM and 4.05 µM). We also identified scopafungin as a novel positive allosteric modulator of hP2X7. Screening a traditional medicinal plant extract library revealed 39 plant species with inhibitory action at hP2X7 and 17 plant species with positive allosteric modulator activity. Using computational docking to filter identified components from these plant species and determine potential antagonists, we investigated nine purified chemicals including flavonoids quercetin, kaempferol, ECG, and EGCG. These were shown to inhibit ATP-induced YO-PRO-1 uptake into HEK-hP2X7 cells; however, we also showed that all four flavonoids demonstrated significant assay interference using a cell-free DNA YO-PRO-1 fluorescence test. One plant extract, Dioscorea nipponica, demonstrating positive modulator activity was investigated, and dioscin was identified as a glycoside with PAM activity in ATP-induced YO-PRO-1 uptake assay and whole-cell patch-clamp recordings. However, membrane permeabilisation was observed following application > 10 min limiting the use of dioscin as a pharmacological tool. This work describes a useful workflow with multiple assays for the identification of novel allosteric modulators for human P2X7.

由于 P2X7 在炎症信号传导中的作用,它已成为多种疾病的新兴治疗靶点。本研究旨在利用传统医学中使用的植物的独特化学库,从天然来源中发现新型异构调节剂。我们从 NCI 天然产物库中发现了几种 P2X7 拮抗剂化合物,包括 confertifolin 和 digallic acid(IC50 值分别为 3.86 µM 和 4.05 µM)。我们还发现莨菪亭是一种新型的 hP2X7 正异构调节剂。通过筛选传统药用植物提取物库,我们发现 39 种植物对 hP2X7 具有抑制作用,17 种植物具有正异构调节剂活性。我们利用计算对接技术从这些植物物种中筛选出确定的成分并确定潜在的拮抗剂,研究了九种纯化的化学物质,包括黄酮类化合物槲皮素、山柰酚、ECG 和 EGCG。结果表明,这些物质能抑制 ATP 诱导的 HEK-hP2X7 细胞对 YO-PRO-1 的摄取;不过,我们还发现,使用无细胞 DNA YO-PRO-1 荧光测试法,所有四种黄酮类化合物都表现出明显的检测干扰。在 ATP 诱导的 YO-PRO-1 摄取试验和全细胞膜片钳记录中,我们研究了一种具有积极调节活性的植物提取物薯蓣皂苷,并确定薯蓣皂苷具有 PAM 活性。然而,在应用 > 10 分钟后观察到膜渗透,这限制了 dioscin 作为药理学工具的应用。这项研究介绍了一种有用的工作流程,它采用多种检测方法来鉴定新型的人类 P2X7 异位调节剂。
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引用次数: 0
P2X7 receptor in macrophage polarization and its implications in neuroblastoma tumor behavior. 巨噬细胞极化中的 P2X7 受体及其对神经母细胞瘤肿瘤行为的影响
IF 3 4区 医学 Q2 NEUROSCIENCES Pub Date : 2024-10-19 DOI: 10.1007/s11302-024-10051-w
Carolina Adriane Bento, Vanessa Fernandes Arnaud-Sampaio, Talita Glaser, Elena Adinolfi, Robson Coutinho-Silva, Henning Ulrich, Claudiana Lameu

Tumor-associated macrophages (TAMs) exhibit antitumor or protumor responses related to inflammatory (or M1) and alternative (or M2) phenotypes, respectively. The P2X7 receptor plays a key role in macrophage polarization, influencing inflammation and immunosuppression. In this study, we investigated the role of the P2X7 receptor in TAMs. Using P2X7 receptor-deficient macrophages, we analyzed gene expression profiles and their implications for neuroblastoma invasion and chemoresistance. Our results showed that P2X7 receptor deficiency altered the expression of classical polarization markers, such as nitric oxide synthase 2 (Nos2) and tumor necrosis factor-α (Tnf), as well as alternative phenotype markers, including mannose receptor C-type 1 (Mrc1) and arginase 1 (Arg1). P2X7 deficiency also influenced the expression of the ectonucleotidases Entpd1 and Nt5e and other purinergic receptors, especially P2ry2, suggesting compensatory mechanisms involved in macrophage polarization. In particular, TAMs deficient in P2X7 showed a phenotype with characteristics intermideiate between resting macrophages (M0) and M1 polarization rather than the M2-type phenotype like and wild-type TAM macrophages. In addition, P2rx7-/- TAMs regulated the expression of P2X7 receptor isoforms in neuroblastoma cells, with downregulation of the P2X7 A and B isoforms leading to a decrease in chemotherapy-induced cell death. However, TAMs expressing P2X7 downregulated only the B isoform, suggesting that TAMs play a role in modulating tumor behavior through P2X7 receptor isoform regulation. Taken together, our data underscore the regulatory function of the P2X7 receptor in orchestrating alternative macrophage polarization and in the interplay between tumor cells and TAMs. These findings help to clarify the complex interplay of purinergic signaling in cancer progression and open up avenues for future research and therapeutic interventions.

肿瘤相关巨噬细胞(TAMs)表现出的抗肿瘤或原肿瘤反应分别与炎症(或 M1)和替代(或 M2)表型有关。P2X7 受体在巨噬细胞极化、影响炎症和免疫抑制中起着关键作用。在这项研究中,我们研究了 P2X7 受体在 TAMs 中的作用。利用 P2X7 受体缺陷的巨噬细胞,我们分析了基因表达谱及其对神经母细胞瘤侵袭和化疗抗性的影响。我们的研究结果表明,P2X7受体缺乏会改变一氧化氮合酶2(Nos2)和肿瘤坏死因子-α(Tnf)等经典极化标记物以及甘露糖受体C型1(Mrc1)和精氨酸酶1(Arg1)等替代表型标记物的表达。P2X7 缺乏也会影响外切核苷酸酶 Entpd1 和 Nt5e 以及其他嘌呤能受体(尤其是 P2ry2)的表达,这表明巨噬细胞极化过程中存在补偿机制。特别是,缺乏 P2X7 的 TAM 表现出介于静息巨噬细胞(M0)和 M1 极化之间的表型,而不是像野生型 TAM 巨噬细胞那样的 M2 型表型。此外,P2rx7-/-TAMs 还能调节神经母细胞瘤细胞中 P2X7 受体同工酶的表达,P2X7 A 和 B 同工酶的下调会导致化疗诱导的细胞死亡减少。然而,表达 P2X7 的 TAMs 只下调 B 异构体,这表明 TAMs 在通过 P2X7 受体异构体调节肿瘤行为方面发挥作用。综上所述,我们的数据强调了 P2X7 受体在协调巨噬细胞替代性极化以及肿瘤细胞与 TAMs 相互作用中的调控功能。这些发现有助于阐明嘌呤能信号在癌症进展中的复杂相互作用,并为未来的研究和治疗干预开辟了道路。
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引用次数: 0
P2 purinergic receptor expression and function in tumor-related immune cells. 肿瘤相关免疫细胞中 P2 嘌呤能受体的表达和功能。
IF 3 4区 医学 Q2 NEUROSCIENCES Pub Date : 2024-10-10 DOI: 10.1007/s11302-024-10054-7
Vahinipriya Manoharan, Oluwafemi O Adegbayi, Janielle P Maynard

P2 purinergic receptor expression is dysregulated in multiple cancer subtypes and is associated with worse outcomes. Studies identify roles for P2 purinergic receptors in tumor cells that drive disease aggressiveness. There is also sufficient evidence that P2 purinergic receptor expression within the tumor microenvironment (TME) is critical for disease initiation and progression. Immune cells constitute a significant component of the TME and display both tumorigenic and anti-tumorigenic potential. Studies pre-dating the investigation of P2 purinergic receptors in cancer identify P2 receptor expression on multiple immune cells including macrophages, neutrophils, T-cells, and dendritic cells; all of which are implicated in tumor initiation, tumor promotion, or response to treatment. Herein, we discuss P2 purinergic receptor expression and function in tumor-related immune cells. We provide a rationale for further investigations of P2 purinergic receptors within the TME to better define the mechanistic pathways of inflammation-mediate tumorigenesis and explore P2 purinergic receptors as potential targets for novel immunotherapeutic approaches.

P2 嘌呤能受体在多种癌症亚型中表达失调,并与恶化的预后有关。研究发现,P2嘌呤能受体在肿瘤细胞中起着驱动疾病侵袭性的作用。还有充分证据表明,P2嘌呤能受体在肿瘤微环境(TME)中的表达对疾病的发生和发展至关重要。免疫细胞是肿瘤微环境的重要组成部分,具有致瘤和抗肿瘤的潜能。在对癌症中的 P2 嘌呤能受体进行调查之前的研究发现,多种免疫细胞(包括巨噬细胞、中性粒细胞、T 细胞和树突状细胞)上都有 P2 受体的表达;所有这些细胞都与肿瘤的诱发、肿瘤的促进或对治疗的反应有关。在此,我们将讨论 P2 嘌呤能受体在肿瘤相关免疫细胞中的表达和功能。我们为进一步研究 TME 中的 P2 嘌呤能受体提供了理论依据,以更好地界定炎症介导肿瘤发生的机理途径,并探索 P2 嘌呤能受体作为新型免疫治疗方法潜在靶点的可能性。
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引用次数: 0
Heterologous expression and biochemical characterization of the recombinant nucleoside triphosphate diphosphohydrolase 2 (LbNTPDase2) from Leishmania (Viannia) braziliensis. 巴西利什曼原虫重组核苷三磷酸二磷酸水解酶2 (LbNTPDase2)的异源表达及生化特性研究。
IF 3 4区 医学 Q2 NEUROSCIENCES Pub Date : 2024-10-01 Epub Date: 2023-11-24 DOI: 10.1007/s11302-023-09980-9
Nancy da Rocha Torres Pavione, João Victor Badaró de Moraes, Isadora Cunha Ribeiro, Raissa Barbosa de Castro, Walmir da Silva, Anna Cláudia Alves de Souza, Victor Hugo Ferraz da Silva, Raphael de Souza Vasconcellos, Gustavo da Costa Bressan, Juliana Lopes Rangel Fietto

Leishmania braziliensis is a pathogenic protozoan parasite that causes American Tegumentary Leishmaniasis (ATL), an important tropical neglected disease. ENTPDases are nucleotidases that hydrolyze intracellular and/or extracellular nucleotides. ENTPDases are known as regulators of purinergic signalling induced by extracellular nucleotides. Leishmania species have two isoforms of ENTPDase, and, particularly, ENTPDase2 seems to be involved in infectivity and virulence. In this study, we conducted the heterologous expression and biochemical characterization of the recombinant ENTPDase2 of L. braziliensis (rLbNTPDase2). Our results show that this enzyme is a canonical ENTPDase with apyrase activity, capable of hydrolysing triphosphate and diphosphate nucleotides, and it is dependent on divalent cations (calcium or magnesium). Substrate specificity was characterized as UDP>GDP>ADP>GTP>ATP=UTP. The enzyme showed optimal activity at a neutral to basic pH and was partially inhibited by suramin and DIDS. Furthermore, the low apparent Km for ADP suggests that the enzyme may play a role in adenosine-mediated signalling. The biochemical characterization of this enzyme can open new avenues for using LbNTPDase2 as a drug target.

巴西利什曼原虫是一种致病的原生动物寄生虫,可引起美洲背生利什曼病(ATL),这是一种重要的热带被忽视疾病。entpase是水解细胞内和/或细胞外核苷酸的核苷酸酶。entpases被认为是细胞外核苷酸诱导的嘌呤能信号的调节因子。利什曼原虫有两种entpase亚型,特别是entpase 2似乎与传染性和毒力有关。在本研究中,我们对巴西乳杆菌重组ENTPDase2 (rLbNTPDase2)进行了异源表达和生化鉴定。我们的研究结果表明,该酶是一种典型的具有apyrase活性的entpase,能够水解三磷酸和二磷酸核苷酸,并且依赖于二价阳离子(钙或镁)。底物特异性表现为UDP>GDP>ADP>GTP>ATP=UTP。该酶在中性至碱性pH下表现出最佳活性,并被苏拉明和DIDS部分抑制。此外,ADP的低表观Km表明该酶可能在腺苷介导的信号传导中发挥作用。该酶的生化特性为利用LbNTPDase2作为药物靶点开辟了新的途径。
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引用次数: 0
Role of CD73 and the purinergic signaling pathway in the pathogenesis of fusion-negative rhabdomyosarcoma. CD73和嘌呤能信号通路在融合阴性横纹肌肉瘤发病机制中的作用
IF 3 4区 医学 Q2 NEUROSCIENCES Pub Date : 2024-10-01 Epub Date: 2024-05-03 DOI: 10.1007/s11302-024-10013-2
Amelia Fascì, Silvia Deaglio
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引用次数: 0
Promoting glymphatic flow: A non-invasive strategy using 40 Hz light flickering. 促进淋巴流动:使用 40 Hz 灯光闪烁的非侵入性策略。
IF 3 4区 医学 Q2 NEUROSCIENCES Pub Date : 2024-10-01 DOI: 10.1007/s11302-024-10052-9
Jianchen Fan, Zhihua Gao

The glymphatic system is critical for brain homeostasis by eliminating metabolic waste, whose disturbance contributes to the accumulation of pathogenic proteins in neurodegenerative diseases. Promoting glymphatic clearance is a potential and attractive strategy for several brain disorders, including neurodegenerative diseases. Previous studies have uncovered that 40 Hz flickering augmented glymphatic flow and facilitated sleep (Zhou et al. in Cell Res 34:214-231, 2024) since sleep drives waste clearance via glymphatic flow (Xie et al. in Science 342:373-377, 2013). However, it remains unclear whether 40 Hz light flickering directly increased glymphatic flow or indirectly by promoting sleep. A recent article published in Cell Discovery by Chen et al. (Sun et al. in Cell Discov 10:81, 2024) revealed that 40 Hz light flickering facilitated glymphatic flow, by promoting the polarization of astrocytic aquaporin-4 (AQP4) and vasomotion through upregulated adenosine-A2A receptor (A2AR) signaling, independent of sleep. These findings suggest that 40 Hz light flickering may be used as a non-invasive approach to control the function of the glymphatic-lymphatic system, to help remove metabolic waste in the brain, thereby presenting a potential strategy for neurodegenerative disease treatment.

甘油系统通过清除代谢废物对大脑的平衡至关重要,而代谢废物的紊乱会导致神经退行性疾病中致病蛋白质的积累。对于包括神经退行性疾病在内的多种脑部疾病,促进甘油清除是一种具有吸引力的潜在策略。先前的研究发现,40 赫兹的闪烁能增强甘液流并促进睡眠(Zhou 等,发表于《细胞研究》34:214-231,2024 年),因为睡眠能通过甘液流促进废物清除(Xie 等,发表于《科学》342:373-377,2013 年)。然而,目前仍不清楚40赫兹的灯光闪烁是直接增加了脑浆流动,还是通过促进睡眠间接增加了脑浆流动。最近,Chen等人发表在《细胞发现》(Cell Discovery)上的一篇文章(Sun等人,发表于《细胞发现》10:81, 2024)揭示,40赫兹光闪烁通过上调腺苷-A2A受体(A2AR)信号,促进星形胶质细胞水光素-4(AQP4)的极化和血管运动,从而促进甘液流动,与睡眠无关。这些研究结果表明,40 赫兹的灯光闪烁可作为一种非侵入性方法来控制甘液-淋巴系统的功能,帮助清除大脑中的代谢废物,从而为神经退行性疾病的治疗提供一种潜在的策略。
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引用次数: 0
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Purinergic Signalling
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