CNS Neuroscience & Therapeutics最新文献_第6页

Effect of Different Treatments on Retinal Thickness Changes in Patients With Multiple Sclerosis: A Review

IF 4.8 1区医学 Q1 NEUROSCIENCES

CNS Neuroscience & Therapeutics

Pub Date : 2025-01-24 DOI: 10.1111/cns.70225

Armin Adibi, Iman Adibi, Milad Javidan

Background

Multiple sclerosis (MS) is an autoimmune disorder affecting the central nervous system, with varying clinical manifestations such as optic neuritis, sensory disturbances, and brainstem syndromes. Disease progression is monitored through methods like MRI scans, disability scales, and optical coherence tomography (OCT), which can detect retinal thinning, even in the absence of optic neuritis. MS progression involves neurodegeneration, particularly trans-synaptic degeneration, which extends beyond the initial injury site. This review focuses on the impact of different MS treatments on retinal thickness as assessed by OCT.

Results

Injectable drugs, such as interferon beta and glatiramer acetate (GA), have a relatively modest impact on retinal atrophy. Oral medications like Fingolimod, Teriflunomide, and Dimethyl fumarate also have different impacts on retinal thickness. Fingolimod has been shown to protect against retinal thinning but may lead to macular edema. DMF-treated patients had less ganglion cell–inner plexiform layer thinning than GA-treated patients but more thinning compared to natalizumab-treated patients and healthy controls. Teriflunomide's impact on retinal layers remains unexplored in human studies. Monoclonal antibodies, including Alemtuzumab, Rituximab, Ocrelizumab, and Natalizumab, had protective effects on retinal layer atrophy. Alemtuzumab-treated patients showed significantly less atrophy compared to interferon- and GA-treated patients. Rituximab initially increased atrophy rates in the first months but subsequently demonstrated potential neuroprotective effects. Ocrelizumab slowed the rate of inner nuclear layer thinning in progressive forms of the disease. Natalizumab is considered the most effective in reducing retinal layer atrophy, particularly the peripapillary retinal nerve fiber layer.

Conclusions

It's important to note that the effectiveness of these treatments may vary depending on MS subtype and individual factors. Future research should explore the long-term effects of these treatments on retinal layers and their correlations with overall disease progression and disability in MS patients.

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引用次数: 0

Deep-Learning Generated Synthetic Material Decomposition Images Based on Single-Energy CT to Differentiate Intracranial Hemorrhage and Contrast Staining Within 24 Hours After Endovascular Thrombectomy

IF 4.8 1区医学 Q1 NEUROSCIENCES

CNS Neuroscience & Therapeutics

Pub Date : 2025-01-24 DOI: 10.1111/cns.70235

Tianyu Wang, Caiwen Jiang, Weili Ding, Qing Chen, Dinggang Shen, Zhongxiang Ding

Aims

To develop a transformer-based generative adversarial network (trans-GAN) that can generate synthetic material decomposition images from single-energy CT (SECT) for real-time detection of intracranial hemorrhage (ICH) after endovascular thrombectomy.

Materials

We retrospectively collected data from two hospitals, consisting of 237 dual-energy CT (DECT) scans, including matched iodine overlay maps, virtual noncontrast, and simulated SECT images. These scans were randomly divided into a training set (n = 190) and an internal validation set (n = 47) in a 4:1 ratio based on the proportion of ICH. Additionally, 26 SECT scans were included as an external validation set. We compared our trans-GAN with state-of-the-art generation methods using several physical metrics of the generated images and evaluated the diagnostic efficacy of the generated images for differentiating ICH from contrast staining.

Results

In comparison with other generation methods, the images generated by trans-GAN exhibited superior quantitative performance. Meanwhile, in terms of ICH detection, the use of generated images from both the internal and external validation sets resulted in a higher area under the receiver operating characteristic curve (0.88 vs. 0.68 and 0.69 vs. 0.54, respectively) and kappa values (0.83 vs. 0.56 and 0.51 vs. 0.31, respectively) compared with input SECT images.

Conclusion

Our proposed trans-GAN provides a new approach based on SECT for real-time differentiation of ICH and contrast staining in hospitals without DECT conditions.

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引用次数: 0

NOTCH3 Mutation Causes Glymphatic Impairment and Promotes Brain Senescence in CADASIL

IF 4.8 1区医学 Q1 NEUROSCIENCES

CNS Neuroscience & Therapeutics

Pub Date : 2025-01-24 DOI: 10.1111/cns.70140

Chunyi Li, Hui Li, Xuejiao Men, Yuge Wang, Xinmei Kang, Mengyan Hu, Xiaotao Su, Shisi Wang, Danli Lu, Shishi Shen, Huipeng Huang, Xiaohui Deng, Yuxin Liu, Lei Zhang, Wei Cai, Aimin Wu, Zhengqi Lu

Aims

The aim of this study is to investigate the role of glymphatic function of cerebral autosomal dominant arteriopathy, subcortical infarcts, and leukoencephalopathy (CADASIL), the most common monogenic small vessel disease caused by NOTCH3 mutation, and to explore potential therapeutic strategies to improve glymphatic function.

Methods

We assessed glymphatic influx and efflux function in CADASIL mouse models (Notch3^R170C) and correlated these findings with brain atrophy in CADASIL patients. We also investigated the underlying mechanisms of glymphatic impairment, focusing the expression of AQP4 in astrocytic endfeet.

Results

CADASIL mouse exhibited both impaired glymphatic influx and efflux, which impedes waste clearance and promotes brain senescence. In accordance, brain atrophy in CADASIL patients is associated with perivascular space enlargement, indicating that glymphatic impairment contributes to advanced brain senescence in CADASIL. The glymphatic malfunction in CADASIL is attributed to diminished AQP4 expression in astrocytic endfeet, which is the core mediator of glymphatic activity. Mechanistically, AQP4 expression is regulated by NOTCH3-RUNX1-CMYB signaling. Reinforcing AQP4 expression in astrocytes by AAV-based therapy resumes the glymphatic functions in CADASIL mice, which further prevents brain senescence.

Conclusion

We propose that to improve glymphatic function by reinforcing AQP4 expression is a promising therapeutic strategy in CADASIL.

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引用次数: 0

CD4-Derived Double-Negative T Cells Ameliorate Alzheimer's Disease-Like Phenotypes in the 5×FAD Mouse Model

IF 4.8 1区医学 Q1 NEUROSCIENCES

CNS Neuroscience & Therapeutics

Pub Date : 2025-01-23 DOI: 10.1111/cns.70187

Yuanzi Xie, Jing Liu, Zongren Hou, Huan Wang, Kailun Liu, Xiaowei Chen, Zhen Fan, Da Li, Can Li, Yuhualei Pan, Yushang Zhao, Yanbing Zhu, Baoyang Hu

<div> <section> <h3> Background</h3> <p>Alzheimer's disease (AD) is a debilitating neurodegenerative disorder that is difficult to predict and is typically diagnosed only after symptoms manifest. Recently, CD4<sup>+</sup> T cell-derived double-negative T (DNT) cells have shown strong immuno-regulatory properties in both in vitro and in vivo neuronal inflammation studies. However, the effectiveness of DNT cells in treating on AD are not yet fully understood.</p> </section> <section> <h3> Objective</h3> <p>This study's aims were three-fold, to (1) evaluate the efficacy of CD4<sup>+</sup> T cell-derived DNT cells treatment on AD mice, (2) understand how DNT treatment make changes in different cell types of 5FAD mice, (3) identify the side effects of DNT treatment.</p> </section> <section> <h3> Methods</h3> <p>We performed tail vein injection of transformed and amplified CD4<sup>+</sup> T cell-derived DNT cells into 5 × FAD mice, while using WT mice and saline injection 5FAD mice as controls. DNT suspensions or NaCl alone were administered to 5 × FAD mice at the 6 months of age. For intravenous injection (<i>n</i> = 10 for both DNT and control injections), 5 × FAD mice were injected with a total of 5 × 10<sup>6</sup> DNT cells suspended in 200 μL of 0.9% NaCl or 0.9% NaCl alone via the lateral tail vein. Behavioral tests and pathology tests were carried out 30 days after cell transplantation.</p> </section> <section> <h3> Results</h3> <p>Through qualitative analysis, we identified 6 main themes. DNT from young wild-type mice enhance the capability of spatial learning and memory in AD mice. DNT cell treatment rejuvenates the microglial function. DNT cell treatment improves the state of oligodendrocytes. DNT cell treatment finetunes the activation of the immune system. DNT cell treatment improves the synaptic plasticity and increases the complexity of neurons. DNT cell treatment reduces the density of amyloid Beta plaques deposition in the cortex and hippocampus of 5 × FAD mice.</p> </section> <section> <h3> Discussion</h3> <p>The findings from this study reveal that DNT treatment improved spatial memory and learning abilities, reduced Aβ deposition, and enhanced synaptic plasticity, contrasting with previous reports on thymus-derived DNT cells. Additionally, CD4<sup>+</sup> T cell-derived DNT therapy exhibited anti-inflammatory effects and modulated microglial function, promoting a neuroprotective environment. Notably, DNT treatment also reduced tau pat

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引用次数: 0

Molecular Symphony of Mitophagy: Ubiquitin-Specific Protease-30 as a Maestro for Precision Management of Neurodegenerative Diseases

IF 4.8 1区医学 Q1 NEUROSCIENCES

CNS Neuroscience & Therapeutics

Pub Date : 2025-01-22 DOI: 10.1111/cns.70192

Ankit Siwach, Harit Patel, Amit Khairnar, Pathik Parekh

Introduction

Mitochondrial dysfunction stands as a pivotal feature in neurodegenerative disorders, spurring the quest for targeted therapeutic interventions. This review examines Ubiquitin-Specific Protease 30 (USP30) as a master regulator of mitophagy with therapeutic promise in Alzheimer's disease (AD) and Parkinson's disease (PD). USP30's orchestration of mitophagy pathways, encompassing PINK1-dependent and PINK1-independent mechanisms, forms the crux of this exploration.

Method

A systematic literature search was conducted in PubMed, Scopus, and Web of Science, selecting studies that investigated USP's function, inhibitor design, or therapeutic efficacy in AD and PD. Inclusion criteria encompassed mechanistic and preclinical/clinical data, while irrelevant or duplicate references were excluded. Extracted findings were synthesized narratively.

Results

USP30 modulates interactions with translocase of outer mitochondrial membrane (TOM) 20, mitochondrial E3 ubiquitin protein ligase 1 (MUL1), and Parkin, thus harmonizing mitochondrial quality control. Emerging novel USP30 inhibitors, racemic phenylalanine derivatives, N-cyano pyrrolidine, and notably, benzosulphonamide class compounds, restore mitophagy, and reduce neurodegenerative phenotypes across diverse models with minimal off-target effects. Modulation of other USPs also influences neurodegenerative disease pathways, offering additional therapeutic avenues.

Conclusions

In highlighting the nuanced regulation of mitophagy by USP30, this work heralds a shift toward more precise and effective treatments, paving the way for a new era in the clinical management of neurodegenerative disorders.

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引用次数: 0

The Association Between Aspartate Transaminase to Alanine Transaminase Ratio and Perioperative Ischemic Stroke in Patients With Diabetes: A Retrospective Cohort Study 谷草转氨酶与丙氨酸转氨酶比值与糖尿病患者围手术期缺血性卒中的相关性：一项回顾性队列研究。

IF 4.8 1区医学 Q1 NEUROSCIENCES

CNS Neuroscience & Therapeutics

Pub Date : 2025-01-21 DOI: 10.1111/cns.70223

Siyuan Liu, Binbin Wang, Libin Ma, Huikai Yang, Min Liu, Yuxiang Song, Zhikang Zhou, Jingsheng Lou, Daming Zhou, Jiangbei Cao, Yanhong Liu, Weidong Mi, Yulong Ma

Background

Patients with diabetes are at a high risk for perioperative ischemic stroke (PIS). The use of biomarkers to identify high-risk patients and predict PIS may provide considerable reference value in clinical decision-making. The aspartate transaminase/alanine transaminase ratio (De Ritis ratio) has been proven to be associated with specific diabetic complications. However, the association between the De Ritis ratio and PIS has not been evaluated in this population. This retrospective cohort study aimed to evaluate the association between the preoperative De Ritis ratio and PIS in patients with type 2 diabetes undergoing noncardiovascular surgery.

Methods

Data from surgical patients were collected from January 2008 to August 2019. A total of 27,643 patients with type 2 diabetes mellitus (DM) undergoing noncardiovascular surgery under general anesthesia were screened. The optimal De Ritis ratio cutoff value was identified using the receiver operating characteristic (ROC) curve. Logistic regression models were used to evaluate the association between the preoperative De Ritis ratio and PIS. Propensity score matching (PSM), sensitivity analyses, and subgroup analyses were performed to further validate the robustness of this association.

Results

A total of 151 patients experienced PIS. A De Ritis ratio ≥ 1.04 was associated with an elevated risk of PIS after adjusting for baseline characteristics (OR [95% CI]: 2.25 [1.59–3.21]; p < 0.001), intraoperative parameters (2.50 [1.80–3.49]; p < 0.001), and all confounding variables (2.29 [1.61–3.29]; p < 0.001). In the propensity score-matched cohort, the association between the De Ritis ratio and PIS remained significant (2.04 [1.38–3.05]; p < 0.001). These associations were also consistently maintained in the sensitivity and subgroup analyses.

Conclusions

An elevated De Ritis ratio is strongly associated with a higher risk of PIS in patients with type 2 DM undergoing noncardiovascular surgery. This may provide additional information on PIS risk assessment in patients with type 2 DM undergoing noncardiovascular surgery.

背景：糖尿病患者是围手术期缺血性卒中（PIS）的高危人群。利用生物标志物识别高危患者并预测PIS可能对临床决策提供相当大的参考价值。天冬氨酸转氨酶/丙氨酸转氨酶比值（De Ritis ratio）已被证实与特定的糖尿病并发症有关。然而，在这一人群中，De - Ritis比率与PIS之间的关系尚未得到评估。本回顾性队列研究旨在评估接受非心血管手术的2型糖尿病患者术前De - Ritis比率与PIS之间的关系。方法：收集2008年1月至2019年8月手术患者的数据。在全麻下接受非心血管手术的2型糖尿病（DM）患者共27,643例。采用受试者工作特征（ROC）曲线确定最佳德里斯比临界值。采用Logistic回归模型评估术前De - Ritis ratio与PIS之间的关系。进行倾向评分匹配（PSM）、敏感性分析和亚组分析以进一步验证这种关联的稳健性。结果：151例患者出现PIS。在调整基线特征后，De - Ritis ratio≥1.04与PIS风险升高相关(OR [95% CI]: 2.25 [1.59-3.21]；结论：在接受非心血管手术的2型糖尿病患者中，德炎比率升高与PIS的高风险密切相关。这可能为接受非心血管手术的2型糖尿病患者的PIS风险评估提供额外的信息。

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引用次数: 0

Modulating Anxiety-Like Behaviors in Neuropathic Pain: Role of Anterior Cingulate Cortex Astrocytes Activation 神经性疼痛中焦虑样行为的调节：前扣带皮层星形胶质细胞激活的作用。

IF 4.8 1区医学 Q1 NEUROSCIENCES

CNS Neuroscience & Therapeutics

Pub Date : 2025-01-21 DOI: 10.1111/cns.70227

Qingqing Zhou, Qi Zhong, Zhuang Liu, Ziyue Zhao, Jie Wang, Zongze Zhang

Aims

The comorbidity of anxiety-like symptoms in neuropathic pain (NP) is a significant yet often overlooked health concern. Anxiety sufferers may have a lower tolerance for pain, but which is difficult to treat. Accumulating evidence suggests a strong link between astrocytes and the manifestation of NP with concurrent anxiety-like behaviors. And the anterior cingulate cortex (ACC) has emerged as a key player in pain modulation and related emotional processing. However, the complex mechanisms that astrocytes in ACC influence anxiety behavior in mouse models of NP remain largely unexplored.

Methods

Utilizing the traditional spared nerve injury (SNI) surgical model, we employed chemogenetic approaches, immunofluorescence, and western blot to investigate the functional significance and interactive dynamics between ACC astrocytes and excitatory neurons.

Results

Our results revealed that SNI surgery induces NP and delayed anxiety-like behaviors, accompanied by increased astrocyte activity in the ACC. Chemogenetic manipulation demonstrated that inhibiting astrocytes alleviates anxiety symptoms, while activating them exacerbates anxiety-like behaviors, affecting local excitatory neurons and synapse density. Direct manipulation of ACC excitatory neurons also significantly impacted anxiety-like behaviors.

Conclusion

Our results highlight the pivotal role of ACC astrocytes in modulating anxiety-like behavior, suggesting a novel therapeutic strategy for anxiety associated with NP by targeting astrocyte function.

目的：神经性疼痛（NP）中焦虑样症状的共病是一个重要但经常被忽视的健康问题。焦虑患者可能对疼痛的耐受力较低，但这很难治疗。越来越多的证据表明星形胶质细胞与NP的表现与并发的焦虑样行为之间存在密切的联系。前扣带皮层（ACC）在疼痛调节和相关情绪处理中起着关键作用。然而，ACC中的星形胶质细胞影响NP小鼠焦虑行为的复杂机制在很大程度上仍未被探索。方法：利用传统的SNI手术模型，采用化学发生、免疫荧光、western blot等方法研究ACC星形胶质细胞与兴奋性神经元的功能意义及相互作用动力学。结果：我们的研究结果显示SNI手术诱导NP和延迟焦虑样行为，并伴有ACC中星形胶质细胞活性增加。化学发生操作表明，抑制星形胶质细胞可缓解焦虑症状，而激活它们会加剧焦虑样行为，影响局部兴奋性神经元和突触密度。直接操纵ACC兴奋性神经元也显著影响焦虑样行为。结论：我们的研究结果突出了ACC星形胶质细胞在调节焦虑样行为中的关键作用，为靶向星形胶质细胞功能治疗NP相关焦虑提供了一种新的治疗策略。

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引用次数: 0

Evaluating Brain Activity in Patients With Chronic Disorders of Consciousness After Traumatic Brain Injury Using EEG Microstate Analysis During Hyperbaric Oxygen Therapy 高压氧治疗期间脑电图微状态分析评价创伤性脑损伤后慢性意识障碍患者的脑活动。

IF 4.8 1区医学 Q1 NEUROSCIENCES

CNS Neuroscience & Therapeutics

Pub Date : 2025-01-20 DOI: 10.1111/cns.70220

Long Xu, Jiameng Wang, Cong Wang, Qianqian Ge, Ziqi Ren, Chen He, Yun Liu, Bo Wang, Yaling Liu, Lianbi Xue, Jianghong He, Xudong Zhao, Qiuhong Yu

Background

Hyperbaric oxygen (HBO) therapy is an efficacious intervention for patients with prolonged disorders of consciousness (pDOC). Electroencephalographic (EEG) microstate analysis can provide an assessment of the global state of the brain. Currently, the misdiagnosis rate of consciousness-level assessments in patients with pDOC is high. Therefore, we aimed to assess the consciousness levels and outcomes of patients by analyzing changes in EEG signals during HBO therapy.

Methods

EEG data were collected from 32 patients with traumatic brain injury before and after 20 min of HBO therapy. EEG data were obtained during HBO therapy sessions. Modified k-means clustering was used to segment EEG signals into microstates. A paired sample t test was used to compare the microstate characteristics before and during HBO therapy.

Results

The duration, occurrence, and coverage of microstate D significantly increased in the minimally conscious state (MCS) group after therapy. Significant increases in the same parameters were observed in microstate A among patients in the unresponsive wakefulness state group. Furthermore, patients with greater improvements in Coma Recovery Scale-Revised scores (i.e., improvements of more than three points) showed significant increases in the duration, occurrence, and coverage of microstate D. Both the MCS group and the improvement group presented significant increases in the duration, occurrence, and coverage of microstate D during therapy.

Conclusions

Microstate D may be associated with the recovery of consciousness levels in patients. This study verified the safety and feasibility of real-time EEG during HBO therapy for patients with pDOC. The changes in EEG microstate characteristics during HBO therapy can serve as a significant complement to electroencephalographic assessment indices for patients with pDOC and may be useful for predicting the recovery of consciousness levels.

背景：高压氧（HBO）治疗是延长性意识障碍（pDOC）患者的有效干预手段。脑电图（EEG）微观状态分析可以提供对大脑整体状态的评估。目前，pDOC患者意识水平评估的误诊率较高。因此，我们旨在通过分析HBO治疗过程中脑电图信号的变化来评估患者的意识水平和预后。方法：收集32例颅脑外伤患者HBO治疗前后20 min的脑电图资料。在HBO治疗期间获得脑电图数据。采用改进的k-means聚类方法对脑电信号进行微观状态分割。采用配对样本t检验比较HBO治疗前后患者的微状态特征。结果：微状态D在MCS组治疗后持续时间、发生率和覆盖范围均显著增加。在无反应清醒状态组的患者中，在微状态A中观察到相同参数的显著增加。此外，昏迷恢复量表修正评分改善较大（即改善3分以上）的患者在治疗期间微状态D的持续时间、发生次数和覆盖范围均显著增加。MCS组和改善组在治疗期间微状态D的持续时间、发生次数和覆盖范围均显著增加。结论：微状态D可能与患者意识水平的恢复有关。本研究验证了实时脑电图在pDOC患者HBO治疗期间的安全性和可行性。HBO治疗期间脑电图微状态特征的变化可作为pDOC患者脑电图评估指标的重要补充，并可用于预测患者意识水平的恢复。

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引用次数: 0

Correction to “Cinchonine and Cinchonidine Alleviate Cisplatin-Induced Ototoxicity by Regulating PI3K-AKT Signaling” 更正“Cinchonine和Cinchonidine通过调节PI3K-AKT信号减轻顺铂诱导的耳毒性”。

IF 4.8 1区医学 Q1 NEUROSCIENCES

CNS Neuroscience & Therapeutics

Pub Date : 2025-01-20 DOI: 10.1111/cns.70228

D. Tang, X. Wang, J. Wu, Y. Li, C. Li, X. Qiao, L. Fan, Y. Chen, H. Zhu, Z. Zhang, and Y. He, “Cinchonine and Cinchonidine Alleviate Cisplatin-Induced Ototoxicity by Regulating PI3K-AKT Signaling,” CNS Neuroscience & Therapeutics 30, no. 2 (2024): e14403, https://doi.org/10.1111/cns.14403.

We apologize for this error.

引用次数: 0

Electroacupuncture Pretreatment Reduces Ischemic Brain Injury by Inhibiting the Lactate Production and Its Derived Protein Lactylation Formation 电针预处理通过抑制乳酸生成及其衍生蛋白乳酸化形成减少缺血性脑损伤。

IF 4.8 1区医学 Q1 NEUROSCIENCES

CNS Neuroscience & Therapeutics

Pub Date : 2025-01-20 DOI: 10.1111/cns.70231

Xin-Ru Pan, Yao-Dan Zhang, Yuan-Hui Gan, Jia-Hang Zhang, Su-Jin Gao, Xiao-Shuang Feng, Jia-Xin Xie, Yu-Fei Wang, Xin-Xiao Zhang, Peng-Fei Wang, Shu-Guang Yu, Yong Tang, Xiao-Yi Xiong

Aim

Given that electroacupuncture (EA) pretreatment inhibits lactate production and lactate-derived lysine lactation (Kla) aggravates ischemic brain injury, we aimed to investigate whether the formation of Kla protein is involved in EA pretreatment to alleviate ischemic brain injury.

Methods

EA was performed on the Baihui acupoint (GV20) of male C57BL/6J mice before receiving the permanent middle cerebral artery occlusion (pMCAO) surgery. Western blot and immunofluorescent staining were used to observe neuronal survival, astrocyte activation, and protein Kla levels, and the lactate levels in ischemic brains were assayed with a commercial kit. TTC staining and neurological function scores are performed to evaluate the brain damage in mice.

Results

We found that the increased lactate content and protein Kla levels were significantly decreased in ischemic brain tissue of mice after receiving EA pretreatment, and accompanied by the reduction of astrocyte activation and neuronal injury and death. Meantime, we found that EA pretreatment was effective in reversing the worsening of ischemic brain injury caused by lactate supplementation. However, EA pretreatment did not further reduce the lactate content and protein Kla levels and ameliorate brain injury in ischemic stroke mice after inhibition of glycolysis.

Conclusion

Our study reveals that EA pretreatment reduced ischemic brain damage by inhibiting lactate production and its derived protein Kla formation in mice with ischemic stroke.

目的：鉴于电针（EA）预处理抑制乳酸生成，乳酸源性赖氨酸泌乳（Kla）加重缺血性脑损伤，我们旨在探讨Kla蛋白的形成是否参与电针预处理对缺血性脑损伤的缓解作用。方法：在C57BL/6J雄性小鼠永久性大脑中动脉闭塞（pMCAO）手术前，对其百会穴（GV20）进行电刺激。采用Western blot和免疫荧光染色法观察神经元存活、星形胶质细胞活化、蛋白Kla水平，并用商品化试剂盒检测缺血脑组织乳酸水平。采用TTC染色和神经功能评分评价小鼠脑损伤。结果：我们发现EA预处理后小鼠缺血脑组织乳酸含量和蛋白Kla水平明显降低，并伴有星形胶质细胞活化和神经元损伤死亡的减少。同时，我们发现EA预处理能有效逆转乳酸补充引起的缺血性脑损伤恶化。然而，EA预处理并没有进一步降低糖酵解抑制后缺血性脑卒中小鼠的乳酸含量和蛋白Kla水平，也没有改善脑损伤。结论：我们的研究表明，EA预处理通过抑制缺血性脑卒中小鼠乳酸生成及其衍生蛋白Kla的形成来减轻缺血性脑损伤。

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引用次数: 0