Neurochemistry international最新文献_第8页

Drug delivery based exosomes uptake pathways 基于外泌体摄取途径的药物输送。

IF 4.4 3区医学

Neurochemistry international Pub Date : 2024-08-13 DOI: 10.1016/j.neuint.2024.105835

Moataz Dowaidar

{"title":"Drug delivery based exosomes uptake pathways","authors":"Moataz Dowaidar","doi":"10.1016/j.neuint.2024.105835","DOIUrl":"10.1016/j.neuint.2024.105835","url":null,"abstract":"<div><p>Most cells secrete a material called extracellular vesicles (EVs), which play a crucial role in cellular communication. Exosomes are one of the most studied types of EVs. Recent research has shown the many functions and substrates of cellular exosomes. Multiple studies have shown the efficacy of exosomes in transporting a wide variety of cargo to their respective target cells. As a result, they are often utilized to transport medicaments to patients. Natural exosomes as well as exosomes modified with other compounds to enhance transport capabilities have been employed. In this article, we take a look at how different types of exosomes and modified exosomes may transport different types of cargo to their respective targets. Exosomes have a lot of potential as drug delivery vehicles for many synthetic compounds, proteins, nucleic acids, and gene repair specialists because they can stay in the body for a long time, are biocompatible, and can carry natural materials. A good way to put specific protein particles into exosomes is still not clear, though, and the exosomes can't be used in many situations yet. The determinants for exosome production, as well as ways for loading certain therapeutic molecules (proteins, nucleic acids, and small compounds), were covered in this paper. Further study and the development of therapeutic exosomes may both benefit from the information collected in this review.</p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"179 ","pages":"Article 105835"},"PeriodicalIF":4.4,"publicationDate":"2024-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141987112","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

ISRIB ameliorates spatial learning and memory impairment induced by adolescent intermittent ethanol exposure in adult male rats ISRIB 可改善成年雄性大鼠因青少年间歇性接触乙醇而导致的空间学习和记忆损伤。

IF 4.4 3区医学

Neurochemistry international Pub Date : 2024-08-12 DOI: 10.1016/j.neuint.2024.105834

Wenge Jia , Chenchen Li , Hongyun Chen , Xinyu Wang , Yuan Liu , Wanbing Shang , Bian Wang , Wenjing Meng , Yaxin Guo , Lijie Zhu , Dan Wang , Danya Zhou , Bin Zhao , Lai Wei

{"title":"ISRIB ameliorates spatial learning and memory impairment induced by adolescent intermittent ethanol exposure in adult male rats","authors":"Wenge Jia , Chenchen Li , Hongyun Chen , Xinyu Wang , Yuan Liu , Wanbing Shang , Bian Wang , Wenjing Meng , Yaxin Guo , Lijie Zhu , Dan Wang , Danya Zhou , Bin Zhao , Lai Wei","doi":"10.1016/j.neuint.2024.105834","DOIUrl":"10.1016/j.neuint.2024.105834","url":null,"abstract":"<div><p>Alcohol exposure in adolescence is considered a major cause of cognitive impairments later in life including spatial learning and memory. Integrated stress response (ISR), a program of conservative translation and transcription, is crucial in synaptic plasticity and memory. Although previous studies have elucidated ISR in different brain areas involved in learning and memory disorders, the impact of ISR on learning and memory following adolescent alcohol exposure remains unclear. Here, we demonstrated that adolescent intermittent ethanol (AIE) exposure caused spatial learning and memory impairment, combined with neuronal damage in the medial prefrontal cortex (mPFC), nucleus accumbens (NAc) and hippocampus (HIP) in adult rats. Moreover, integrated stress response inhibitor (ISRIB) administration not only improved spatial learning and memory impairment and neuronal damage but also inhibited the endoplasmic reticulum stress (ER) and reversed changes in synaptic proteins. These findings suggested that ISRIB ameliorates AIE exposure-induced spatial learning and memory deficits by improving neural morphology and synaptic function through inhibiting ER stress signaling pathway in the mPFC, NAc and HIP in adulthood. Our findings may enhance comprehension of cognitive function and neuronal effects of adolescent ethanol exposure and ISRIB treatment may be an underlying potential option for addressing alcohol-induced learning and memory deficits.</p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"179 ","pages":"Article 105834"},"PeriodicalIF":4.4,"publicationDate":"2024-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141981424","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

Dopaminergic cAMP signaling in mouse olfactory bulb astrocytes 小鼠嗅球星形胶质细胞中的多巴胺能 cAMP 信号转导

IF 4.4 3区医学

Neurochemistry international Pub Date : 2024-08-10 DOI: 10.1016/j.neuint.2024.105828

Levi von Kalben , Jessica Sauer , Christine Gee , Daniela Hirnet , Christian Lohr

{"title":"Dopaminergic cAMP signaling in mouse olfactory bulb astrocytes","authors":"Levi von Kalben , Jessica Sauer , Christine Gee , Daniela Hirnet , Christian Lohr","doi":"10.1016/j.neuint.2024.105828","DOIUrl":"10.1016/j.neuint.2024.105828","url":null,"abstract":"<div><p>Cyclic AMP (cAMP) is an important second messenger in virtually all animal cell types, including astrocytes. In the brain, it modulates energy metabolism, development and synaptic plasticity. Dopamine receptors are G protein-coupled receptors that affect cAMP production by adenylyl cyclases. They are divided into two subgroups, D1-like receptors linked to G<sub>s</sub> proteins stimulating cAMP production and D2-like receptors linked to G<sub>i/o</sub> proteins inhibiting cAMP production. In the present study, we investigated the effect of dopamine receptor activation on cAMP dynamics in astrocytes of the mouse olfactory bulb, the brain region with the largest population of dopaminergic neurons. Using the genetically encoded cAMP sensor Flamindo2 we visualized changes in the cytosolic cAMP concentration and showed that dopamine application results in a transient increase in cAMP. This cAMP increase could be mimicked by the D1-like receptor agonist A 68930 and was inhibited by the D1-like receptor antagonist SCH 23390, whereas D2-like receptor ligands had no effect on the astrocytic cAMP concentration. Thus, olfactory bulb astrocytes express D1-like receptors that are linked to cAMP production.</p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"179 ","pages":"Article 105828"},"PeriodicalIF":4.4,"publicationDate":"2024-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141970281","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

l-theanine, the unique constituent of tea, improves neuronal survivability by curtailing inflammatory responses in MPTP model of Parkinson's disease 茶叶中的独特成分 L-茶氨酸可通过抑制帕金森病 MPTP 模型中的炎症反应来提高神经元的存活率。

IF 4.4 3区医学

Neurochemistry international Pub Date : 2024-08-10 DOI: 10.1016/j.neuint.2024.105830

Satarupa Deb , Anupom Borah

{"title":"l-theanine, the unique constituent of tea, improves neuronal survivability by curtailing inflammatory responses in MPTP model of Parkinson's disease","authors":"Satarupa Deb , Anupom Borah","doi":"10.1016/j.neuint.2024.105830","DOIUrl":"10.1016/j.neuint.2024.105830","url":null,"abstract":"<div><p>Discrete components of tea possess multitude of health advantages. Escalating evidence advocate a consequential association between habitual tea consumption and a subsided risk of Parkinson's disease (PD). <span>l</span>-theanine is a non-protein amino acid inherent in tea plants, which exhibits structural resemblance with glutamate, the copious excitatory neurotransmitter in brain. Neuromodulatory effects of <span>l</span>-theanine are evident from its competency in traversing the blood brain barrier, promoting a sense of calmness beyond enervation, and enhancing cognition and attention. Despite the multifarious reports on antioxidant properties of <span>l</span>-theanine and its potential to regulate brain neurotransmitter levels, it is obligatory to understand its exact contribution in ameliorating the pathophysiology of PD. In this study, MPTP-induced mouse model was established and PD-like symptoms were developed in test animals where an increasing dosage of <span>l</span>-theanine (5, 25, 50, 100 and 250 mg/kg) was intraperitoneally administered for 23 days. 50 and 100 mg/kg dosage of <span>l</span>-theanine alleviated motor impairment and specific non-motor symptoms in Parkinsonian mice. The dosage of 100 mg/kg of <span>l</span>-theanine also improved striatal dopamine and serotonin level and tyrosine-hydroxylase positive cell count in the substantia nigra. Most crucial finding of the study is the proficiency of <span>l</span>-theanine to diminish astroglial injury as well as nitric oxide synthesis, which suggests its possible credential to prevent neurodegeneration by virtue of its anti-inflammatory attribute.</p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"179 ","pages":"Article 105830"},"PeriodicalIF":4.4,"publicationDate":"2024-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141915773","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

Capsaicin-insensitivity of TRPV1-R575D mutant located at the lipid-water-interface region can be rescued by either extracellular Ca2+-chelation or cholesterol reduction 位于脂质-水-界面区域的 TRPV1-R575D 突变体对辣椒素的敏感性可通过细胞外 Ca2+ 螯合或降低胆固醇来挽救。

IF 4.4 3区医学

Neurochemistry international Pub Date : 2024-08-06 DOI: 10.1016/j.neuint.2024.105826

Sushama Mohanta , Nilesh Kumar Das , Somdatta Saha , Chandan Goswami

{"title":"Capsaicin-insensitivity of TRPV1-R575D mutant located at the lipid-water-interface region can be rescued by either extracellular Ca2+-chelation or cholesterol reduction","authors":"Sushama Mohanta , Nilesh Kumar Das , Somdatta Saha , Chandan Goswami","doi":"10.1016/j.neuint.2024.105826","DOIUrl":"10.1016/j.neuint.2024.105826","url":null,"abstract":"<div><p>TRPV1 acts as a unique polymodal ion channel having distinct structure and gating properties. In this context, TRPV1-R575D represents a special mutant located at the inner lipid-water-interface (LWI) region that has less possibility of interaction with membrane cholesterol. In control conditions, this lab-generated mutant of TRPV1 shows no “ligand-sensitivity”, reduced surface expression, reduced localization in the lipid rafts, yet induces high cellular lethality. Notably, the cellular lethality induced by TRPV1-R575D expression can be rescued by adding 5′I-RTX (a specific inhibitor of TRPV1) or by introducing another mutation in the next position, i.e. in TRPV1-R575D/D576R. In this work we characterized TRPV1-R575D and TRPV1-R575D/D576R mutants in different cellular conditions and compared with the TRPV1-WT. We report that the “ligand-insensitivity” of TRPV1-R575D can be rescued in certain conditions, such as by chelation of extracellular Ca<sup>2+</sup>, or by reduction of the membrane cholesterol. Here we show that Ca<sup>2+</sup> plays an important role in the channel gating of TRPV1-WT as well as LWI mutants (TRPV1-R575D, TRPV1-R575D/D576R). However, chelation of intracellular Ca<sup>2+</sup> or depletion of ER Ca<sup>2+</sup> did not have a significant effect on the TRPV1-R575D. Certain properties related to channel gating of mutant TRPV1-R575D/D576R can be rescued partially or fully in a context -dependent manner. Cholesterol depletion also alters these properties. Our data suggests that lower intracellular basal Ca<sup>2+</sup> acts as a pre-requisite for further opening of TRPV1-R575D. These findings enable better understanding of the structure-function relationship of TRPV1 and may be critical in comprehending the channelopathies induced by other homologous thermosensitive TRPVs.</p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"179 ","pages":"Article 105826"},"PeriodicalIF":4.4,"publicationDate":"2024-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141905411","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

The autophagy paradox: A new hypothesis in neurodegenerative disorders 自噬悖论：神经退行性疾病的新假说。

IF 4.4 3区医学

Neurochemistry international Pub Date : 2024-08-05 DOI: 10.1016/j.neuint.2024.105827

Haleh Barmaki , Alireza Nourazarian , Behrouz Shademan , Fatemeh khaki-khatibi

{"title":"The autophagy paradox: A new hypothesis in neurodegenerative disorders","authors":"Haleh Barmaki , Alireza Nourazarian , Behrouz Shademan , Fatemeh khaki-khatibi","doi":"10.1016/j.neuint.2024.105827","DOIUrl":"10.1016/j.neuint.2024.105827","url":null,"abstract":"<div><p>A recent study showed that while autophagy is usually tied to protein and organelle turnover, it can also play dual roles in neurodegenerative diseases. Traditionally, autophagy was seen as protective since it removes damaged proteins and organelles. but new data suggests autophagy can sometimes promote neuron death. and This review tackles autophagy's seemingly contradictory effects in neurodegeneration, or the \"autophagy paradox. \" It offers a framework for understanding autophagy in neurodegenerative research and the cellular processes involved. In short, our data uncovers a harmful autophagy role in certain situations, conflicting the view that it's always beneficial. We describe the distinct, disease-specific autophagy pathways functioning in various neurodegenerative diseases. Part two concerns potential therapeutic implications of manipulating autophagy and current strategies targeting the autophagic system, suggesting interesting areas for future research into tailored modulators. This could eventually enable activating or controlling specific autophagy pathways and aid in developing more effective treatments. Researchers believe more molecular-level research is needed so patient-tailored autophagy-modulating therapeutics can be developed given this dilemma. Moreover, research must translate faster into effective neurodegenerative disease treatment options. This article aims to provide a wholly new perspective on autophagy's classically described role in these severe diseases, challenging current dogma and opening new therapeutic avenue options.</p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"179 ","pages":"Article 105827"},"PeriodicalIF":4.4,"publicationDate":"2024-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141900436","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

The selective disruption of the JNK2/Syntaxin-1A interaction by JGRi1 protects against NMDA-evoked toxicity in SH-SY5Y cells JGRi1 对 JNK2/SYNTAXIN-1A 相互作用的选择性分离可保护 SH-SY5Y 细胞免受 NMDA 引起的毒性。

IF 4.4 3区医学

Neurochemistry international Pub Date : 2024-08-03 DOI: 10.1016/j.neuint.2024.105824

M. Cimino , M. Feligioni

{"title":"The selective disruption of the JNK2/Syntaxin-1A interaction by JGRi1 protects against NMDA-evoked toxicity in SH-SY5Y cells","authors":"M. Cimino , M. Feligioni","doi":"10.1016/j.neuint.2024.105824","DOIUrl":"10.1016/j.neuint.2024.105824","url":null,"abstract":"<div><p>N-methyl-D-aspartate (NMDA) receptors are calcium-permeable ion-channel receptors, specifically activated by glutamate, that permit the activation of specific intracellular calcium-dependent pathways. Aberrant NMDA receptor activation leads to a condition known as excitotoxicity, in which excessive calcium inflow induces apoptotic pathways. To date, memantine is the only NMDA receptor antagonist authorized in clinical practice, hence, a better understanding of the NMDA cascade represents a need to discover novel pharmacological targets.</p><p>We previously reported non-conventional intracellular signaling triggered by which, upon activation, promotes the interaction between JNK2 and STX1A which enhances the rate of vesicular secretion. We developed a cell-permeable peptide, named JGRi1, able to disrupt such interaction, thus reducing vesicular secretion. In this work, to selectively study the effect of JGRi1 in a much simpler system, we employed neuroblastoma cells, SH-SY5Y. We found that SH-SY5Y cells express the components of the NMDA receptor-JNK2 axis and that the NMDA stimulus increases the rate of vesicle release. Both JGRi1 and memantine protected SH-SY5Y cells from NMDA toxicity, but only JGRi1 reduced the interaction between JNK2 and STX1A. Both drugs successfully reduced NMDA-induced vesicle release, although, unlike memantine, JGRi1 did not prevent calcium influx. NMDA treatment induced JNK2 expression, but not JNK1 or JNK3, which was prevented by both JGRi1 and memantine, suggesting that JNK2 may be specifically involved in the response to NMDA.</p><p>In conclusion, being JGRi1 able to protect cells against NMDA toxicity by interfering with JNK2/STX1A interaction, it could be considered a novel pharmacological tool to counteract excitotoxicity.</p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"179 ","pages":"Article 105824"},"PeriodicalIF":4.4,"publicationDate":"2024-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141888038","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

Tumor necrosis factor alpha induces NOX2-dependent reactive oxygen species production in hypothalamic paraventricular nucleus neurons following angiotensin II infusion 输注血管紧张素 II 后，肿瘤坏死因子 alpha 可诱导下丘脑室旁核神经元产生 NOX2 依赖性活性氧。

IF 4.4 3区医学

Neurochemistry international Pub Date : 2024-08-02 DOI: 10.1016/j.neuint.2024.105825

Clara Woods , Gang Wang , Teresa A. Milner , Michael J. Glass

{"title":"Tumor necrosis factor alpha induces NOX2-dependent reactive oxygen species production in hypothalamic paraventricular nucleus neurons following angiotensin II infusion","authors":"Clara Woods , Gang Wang , Teresa A. Milner , Michael J. Glass","doi":"10.1016/j.neuint.2024.105825","DOIUrl":"10.1016/j.neuint.2024.105825","url":null,"abstract":"<div><p>There is evidence that tumor necrosis factor alpha (TNFα) influences autonomic processes coordinated within the hypothalamic paraventricular nucleus (PVN), however, the signaling mechanisms subserving TNFα′s actions in this brain area are unclear. In non-neuronal cell types, TNFα has been shown to play an important role in canonical NADPH oxidase (NOX2)-mediated production of reactive oxygen species (ROS), molecules also known to be critically involved in hypertension. However, little is known about the role of TNFα in NOX2-dependent ROS production in the PVN within the context of hypertension. Using dual labeling immunoelectron microscopy and dihydroethidium (DHE) microfluorography, we provide structural and functional evidence for interactions between TNFα and NOX2 in the PVN. The TNFα type 1 receptor (TNFR1), the major mediator of TNFα signaling in the PVN, was commonly co-localized with the catalytic gp91<sup>phox</sup> subunit of NOX2 in postsynaptic sites of PVN neurons. Additionally, there was an increase in dual labeled dendritic profiles following fourteen-day slow-pressor angiotensin II (AngII) infusion. Using DHE microfluorography, it was also shown that TNFα application resulted in a NOX2-dependent increase in ROS in isolated PVN neurons projecting to the spinal cord. Further, TNFα-mediated ROS production was heightened after AngII infusion. The finding that TNFR1 and gp91<sup>phox</sup> are positioned for rapid interactions, particularly in PVN-spinal cord projection neurons, provides a molecular substrate by which inflammatory signaling and oxidative stress may jointly contribute to AngII hypertension.</p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"179 ","pages":"Article 105825"},"PeriodicalIF":4.4,"publicationDate":"2024-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141888039","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

Diet and Nutraceuticals for treatment and prevention of primary and secondary stroke: Emphasis on nutritional antiplatelet and antithrombotic agents 治疗和预防一级和二级中风的饮食和营养保健品：重点是营养抗血小板和抗血栓药物

IF 4.4 3区医学

Neurochemistry international Pub Date : 2024-07-30 DOI: 10.1016/j.neuint.2024.105823

Ramakrishna Kakarla , Lakshmi Anusha Vinjavarapu , Sairam Krishnamurthy

{"title":"Diet and Nutraceuticals for treatment and prevention of primary and secondary stroke: Emphasis on nutritional antiplatelet and antithrombotic agents","authors":"Ramakrishna Kakarla , Lakshmi Anusha Vinjavarapu , Sairam Krishnamurthy","doi":"10.1016/j.neuint.2024.105823","DOIUrl":"10.1016/j.neuint.2024.105823","url":null,"abstract":"<div><p>Ischemic stroke is a devastating disease that causes morbidity and mortality. Malnutrition following ischemic stroke is common in stroke patients. During the rehabilitation, the death rates of stroke patients are significantly increased due to malnutrition. Nutritional supplements such as protein, vitamins, fish, fish oils, moderate wine or alcohol consumption, nuts, minerals, herbal products, food colorants, marine products, fiber, probiotics and Mediterranean diets have improved neurological functions in stroke patients as well as their quality of life. Platelets and their mediators contribute to the development of clots leading to stroke. Ischemic stroke patients are treated with thrombolytics, antiplatelets, and antithrombotic agents. Several systematic reviews, meta-analyses, and clinical trials recommended that consumption of these nutrients and diets mitigated the vascular, peripheral, and central complications associated with ischemic stroke (Fig. 2). Particularly, these nutraceuticals mitigated the platelet adhesion, activation, and aggregation that intended to reduce the risks of primary and secondary stroke. Although these nutraceuticals mitigate platelet dysfunction, there is a greater risk of bleeding if consumed excessively. Moreover, malnutrition must be evaluated and adequate amounts of nutrients must be provided to stroke patients during intensive care units and rehabilitation periods. In this review, we have summarized the importance of diet and nutraceuticals in ameliorating neurological complications and platelet dysfunction with an emphasis on primary and secondary prevention of ischemic stroke.</p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"179 ","pages":"Article 105823"},"PeriodicalIF":4.4,"publicationDate":"2024-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141795846","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

Exosomal Src from hypoxic vascular smooth muscle cells exacerbates ischemic brain injury by promoting M1 microglial polarization 缺氧血管平滑肌细胞外泌体 Src 通过促进 M1 小胶质细胞极化加剧缺血性脑损伤

IF 4.4 3区医学

Neurochemistry international Pub Date : 2024-07-29 DOI: 10.1016/j.neuint.2024.105819

Xiaoting Zhang , Jingpei Guo , Junbin Liu , Junfeng Liu , Zhaozhu Li , Jiayao Chen , Jiawei Jiang , Ke Zhang , Bin Zhou

{"title":"Exosomal Src from hypoxic vascular smooth muscle cells exacerbates ischemic brain injury by promoting M1 microglial polarization","authors":"Xiaoting Zhang , Jingpei Guo , Junbin Liu , Junfeng Liu , Zhaozhu Li , Jiayao Chen , Jiawei Jiang , Ke Zhang , Bin Zhou","doi":"10.1016/j.neuint.2024.105819","DOIUrl":"10.1016/j.neuint.2024.105819","url":null,"abstract":"<div><p>Inflammatory response mediated by M1 microglia is a crucial factor leading to the exacerbation of brain injury after ischemic stroke (IS). Under the stimulation of IS, vascular smooth muscle cells (VSMCs) switch to the synthetic phenotype characterized by exosome secretion. Previous studies have shown that exosomes play an important role in the regulation of microglial polarization. We reported that exosomes derived from primary human brain VSMCs under hypoxia (HExos), but not those under normoxia (Exos), significantly promoted primary human microglia (HM1900) shift to M1 phenotype. Proteomic analysis showed that the Src protein enriched in HExos was a potential pro-inflammatory mediator. <em>In vitro</em> experiments showed that the expression of Src and M1 markers were upregulated in HM1900 co-incubated with HExos. However, the Src inhibitor dasatinib (DAS) significantly promoted the transformation of HM1900 phenotype from M1 to M2. <em>In vivo</em> experiments of pMCAO mice also revealed that DAS could effectively inhibit the activation of M1 microglia/macrophages, protect neurons from apoptosis, and improve neuronal function. These data suggested that hypoxic-VSMCs-derived exosomes were involved in post-IS inflammation by promoting M1 microglial polarization through Src transmission. Targeting inhibition of Src potentially acts as an effective strategy for treating brain injury after IS.</p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"179 ","pages":"Article 105819"},"PeriodicalIF":4.4,"publicationDate":"2024-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141796702","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