Neuroreport最新文献_第9页

Electroacupuncture improves diabetes-associated cognitive impairment in rats: potential involvement of hippocampal insulin receptor substrates 1/phosphatidylinositol 3-kinase/protein kinase B signaling pathway activation. 电针改善大鼠糖尿病相关认知障碍：海马胰岛素受体底物1/磷脂酰肌醇3-激酶/蛋白激酶B信号通路激活的潜在参与

IF 2.1 4区医学

Neuroreport Pub Date : 2025-12-03 Epub Date: 2025-10-29 DOI: 10.1097/WNR.0000000000002222

Lele Zhang, Hudie Song, Min Ye, Wenjing Kan, Yingju Hu, Hongyu Xie, Aihong Yuan

{"title":"Electroacupuncture improves diabetes-associated cognitive impairment in rats: potential involvement of hippocampal insulin receptor substrates 1/phosphatidylinositol 3-kinase/protein kinase B signaling pathway activation.","authors":"Lele Zhang, Hudie Song, Min Ye, Wenjing Kan, Yingju Hu, Hongyu Xie, Aihong Yuan","doi":"10.1097/WNR.0000000000002222","DOIUrl":"10.1097/WNR.0000000000002222","url":null,"abstract":"Background: Cognitive impairment is highly prevalent in people with diabetes. Electroacupuncture improves diabetes-associated cognitive impairment (DACI), but its regulatory mechanism remains unclear.Methods: The DACI model was established in rats via high-fat diet combined with low-dose intraperitoneal streptozocin. The acupuncture points Yishu (EX-B3), Zusanli (ST36), and Neiting (ST44) were chosen for electroacupuncture therapy. Cognitive function was assessed by Morris water maze test. Staining with hematoxylin and eosin was used to find the pathological changes in the hippocampus. The expression levels of relative proteins were analyzed by Western blot and immunofluorescence. In addition, ELISA was used to measure the levels of lactate and pyruvate in the hippocampus.Results: Electroacupuncture can improve the learning and memory ability of DACI model rats (P<0.01) and hippocampal morphology; electroacupuncture can significantly increase the phosphorylated protein ratios of P-insulin receptor substrates 1 (P-IRS1)/IRS1, P-phosphoinositide 3-kinase (P-PI3K)/PI3K, and P-protein kinase B (P-AKT)/AKT (P < 0.001) and mean fluorescence intensity of P-IRS1, P-PI3K, and P-AKT (P < 0.01); electroacupuncture can promote the expression of glucose transporters (GLUTs) (P < 0.01) and monocarboxylic transporters (MCTs) (P < 0.01) and improves the contents of pyruvate and lactate in the hippocampus of DACI model rats (P < 0.01); Signaling pathway inhibitor LY294002 attenuated the above improvement (P < 0.05).Conclusion: Electroacupuncture's mechanism may be involved in activating the IRS1/PI3K/AKT pathway, promoting the expression of GLUTs and MCTs, and regulating hippocampal energy metabolism.","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":"36 17","pages":"999-1008"},"PeriodicalIF":2.1,"publicationDate":"2025-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12573686/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146011013","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Role of purinergic receptors 2X3 on type II spiral ganglion neurons in the enhancement of medial olivocochlear reflex in mice after long-term noise exposure. ⅱ型螺旋神经节神经元嘌呤能受体2X3在小鼠长期噪声暴露后内侧耳蜗反射增强中的作用。

IF 2.1 4区医学

Neuroreport Pub Date : 2025-12-03 Epub Date: 2025-10-18 DOI: 10.1097/WNR.0000000000002224

Yapeng Li, Peidong Dai, Na Shen, Xinsheng Huang, Dongming Yin

{"title":"Role of purinergic receptors 2X3 on type II spiral ganglion neurons in the enhancement of medial olivocochlear reflex in mice after long-term noise exposure.","authors":"Yapeng Li, Peidong Dai, Na Shen, Xinsheng Huang, Dongming Yin","doi":"10.1097/WNR.0000000000002224","DOIUrl":"10.1097/WNR.0000000000002224","url":null,"abstract":"Objective: This study aimed to elucidate the role of P2X3 receptors on type II spiral ganglion neurons (SGNs) in mediating the enhancement of the medial olivocochlear (MOC) reflex following long-term noise exposure.Methods: We utilized four groups of male CBA/Ca mice: control, ouabain, ouabain noise, and ouabain noise + AF-353. The ouabain group received local cochlear application of ouabain to selectively induce apoptosis of type I SGNs. The ouabain noise group was then exposed to moderate noise [80 dB sound pressure level (SPL)] for 6 h daily over 4 weeks, while the ouabain noise + AF-353 group received the P2X3 receptor blocker AF-353 before noise sessions. Auditory brainstem responses (ABRs) and distortion product otoacoustic emissions (DPOAEs) were measured to assess hearing. The MOC reflex was evaluated via contralateral and ipsilateral suppression of DPOAEs. Immunofluorescence visualized P2X3 receptor expression.Results: Ouabain-treated mice exposed to noise displayed a significantly enhanced MOC reflex, which was attenuated by AF-353. ABR thresholds were elevated and wave I amplitude was reduced, suggesting hearing impairment, whereas DPOAE thresholds were unchanged. Immunofluorescence indicated a marked upregulation of P2X3 receptors in the cochlea's middle turn after noise exposure, an effect decreased by AF-353.Conclusion: The enhanced MOC reflex induced by long-term moderate noise exposure is mediated by the upregulation of P2X3 receptors on type II SGNs. The selective ablation of type I SGNs confirms the pivotal role of type II SGNs in this adaptive neural plasticity.","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":"36 17","pages":"1031-1036"},"PeriodicalIF":2.1,"publicationDate":"2025-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146010923","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Phase coupling in the beta and gamma frequencies of motor cortex activity is elevated in people with Parkinson's disease when medication is temporarily withheld. 帕金森氏症患者在暂时停止服药时，运动皮层活动的β和γ频率的相位耦合会升高。

IF 2.1 4区医学

Neuroreport Pub Date : 2025-12-03 Epub Date: 2025-10-18 DOI: 10.1097/WNR.0000000000002223

Aleksandra S Miasnikova, Elizabeth A Franz

{"title":"Phase coupling in the beta and gamma frequencies of motor cortex activity is elevated in people with Parkinson's disease when medication is temporarily withheld.","authors":"Aleksandra S Miasnikova, Elizabeth A Franz","doi":"10.1097/WNR.0000000000002223","DOIUrl":"10.1097/WNR.0000000000002223","url":null,"abstract":"Objective: How neuronal oscillatory activity in Parkinson's disease (PD) is organized and coordinated is not yet known. We hypothesized that cross-frequency phase synchrony (CFS) in the beta and gamma frequencies measured over the motor cortex [using electroencephalography (EEG)] at rest would be elevated in people with PD compared with healthy controls. ON- versus OFF-medication tests in the PD group were further compared with the hypothesis that elevated CFS would be found in the OFF-medication state.Methods: CFS in beta and gamma frequencies was estimated in EEG recordings from 15 people with mild-moderate Parkinson's and in 15 control participants.Results: Beta-gamma CFS in the motor cortices was increased in the PD OFF tests compared with tests of the control group. As a whole-brain control analysis, large-scale beta-gamma CFS in all 32 channels was found to not differ between groups, thereby isolating abnormal beta-gamma CFS to the motor cortex in PD OFF.Conclusion: New evidence describes brain oscillatory patterns in people with mild-moderate PD, which might pave avenues for early diagnosis and treatments.","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":"36 17","pages":"1025-1030"},"PeriodicalIF":2.1,"publicationDate":"2025-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146010975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Minocycline alleviates mechanical allodynia and modulates hippocampal neuroinflammatory markers in a rat model of neuropathic pain induced by spinal nerve transection. 二甲胺四环素在脊髓神经横断引起的神经性疼痛大鼠模型中减轻机械异常性疼痛并调节海马神经炎症标志物。

IF 2.1 4区医学

Neuroreport Pub Date : 2025-12-03 Epub Date: 2025-10-07 DOI: 10.1097/WNR.0000000000002221

Dandan He, Renfeng Du, Runli Tian, Zhaohui Guo, Qingling Luo, Qinghua Li, Yongnan Li

{"title":"Minocycline alleviates mechanical allodynia and modulates hippocampal neuroinflammatory markers in a rat model of neuropathic pain induced by spinal nerve transection.","authors":"Dandan He, Renfeng Du, Runli Tian, Zhaohui Guo, Qingling Luo, Qinghua Li, Yongnan Li","doi":"10.1097/WNR.0000000000002221","DOIUrl":"10.1097/WNR.0000000000002221","url":null,"abstract":"Objective: This study aimed to investigate the therapeutic effects of minocycline on neuropathic pain by examining its regulatory influence on hippocampal proinflammatory cytokines and brain-derived neurotrophic factor (BDNF) levels, given the established involvement of neuroinflammation and BDNF dysregulation in the pathogenesis of neuropathic pain and associated neurological dysfunctions.Methods: This study used a rat model of neuropathic pain induced by L5 spinal nerve transection (L5-SNT). Forty-eight male Sprague-Dawley rats were divided into four groups: naive, sham-operated, model + saline, and model + minocycline. Minocycline was administered intraperitoneally at 40 mg/kg daily. Mechanical allodynia was assessed using the von Frey test, while real-time reverse transcription and ELISA were employed to quantify hippocampal expression of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), IL-1β, and BDNF at various time points postsurgery.Results: L5-SNT induced significant mechanical allodynia in the model + saline group, which was significantly attenuated by minocycline treatment in the model + minocycline group on days 3, 7, and 11 postsurgery (P < 0.05). Minocycline significantly reduced TNF-α, IL-6, and BDNF levels in the hippocampus, particularly on day 7 post-SNT (P < 0.05); however, minocycline did not significantly affect IL-1β levels. These findings suggest that minocycline's analgesic effects may be mediated through the downregulation of key proinflammatory cytokines and BDNF in the hippocampus.Conclusion: Minocycline administration significantly mitigates mechanical allodynia and modulates hippocampal neuroinflammatory markers in a rat model of neuropathic pain. These results highlight minocycline's potential as a therapeutic option for neuropathic pain, particularly in targeting neuroinflammation within the hippocampus.","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":"36 17","pages":"1016-1024"},"PeriodicalIF":2.1,"publicationDate":"2025-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146010954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

2-Linoleoylglycerol decreased seizure through the regulation of 5-hydroxytryptamine 1A receptor and G protein-coupled receptor 55 interaction in mice. 2-亚油基甘油通过调节5-羟色胺1A受体和G蛋白偶联受体55相互作用减少小鼠癫痫发作。

IF 2.1 4区医学

Neuroreport Pub Date : 2025-12-03 Epub Date: 2025-09-19 DOI: 10.1097/WNR.0000000000002220

Sun Mi Gu, Abdulaziz Jabborov, Jaesuk Yun

{"title":"2-Linoleoylglycerol decreased seizure through the regulation of 5-hydroxytryptamine 1A receptor and G protein-coupled receptor 55 interaction in mice.","authors":"Sun Mi Gu, Abdulaziz Jabborov, Jaesuk Yun","doi":"10.1097/WNR.0000000000002220","DOIUrl":"10.1097/WNR.0000000000002220","url":null,"abstract":"Background: Epilepsy is a central nervous system disorder characterized by abnormal brain activity, leading to seizures or periods of unusual behavior, sensations, and, in some cases, loss of awareness. Cannabidiol, a phytocannabinoid, has recently gained approval as an adjunctive seizure treatment, partly through modulation of G protein-coupled receptor 55 (GPR55), transient receptor potential vanilloid 1, and 5-hydroxytryptamine (5-HT) receptors. Similar to phytocannabinoids, endocannabinoids may also possess therapeutic potential for seizure management; however, no studies have investigated the effects of the endocannabinoid 2-linoleoylglycerol (2-LG). In the present study, we investigated the effects of 2-LG on pentylenetetrazol (PTZ)-induced seizures in mice.Methods: Mice were pretreated with 0 (vehicle), 15, or 30 mg/kg 2-LG intraperitoneally, and saline or 60 mg/kg PTZ was administered 30 min later. Vehicle, WAY-100635 (0.01 mg/kg), or rimonabant (1 mg/kg) were administered 30 min before 2-LG (30 mg/kg) administration, and then saline or 60 mg/kg PTZ was administered 30 min later.Results: Administration of 2-LG (30 mg/kg) significantly reduced seizure scores induced by PTZ. In addition, pretreatment with the 5-HT1A receptor antagonist WAY-100635 reversed the 2-LG antiseizure effect. We also demonstrated that PTZ-induced fluorescence intensity of the GPR55 ligand T1117 in the hippocampus was decreased by 2-LG treatment, and this effect was reversed by WAY-100635 pretreatment. Similarly, the cannabinoid receptor type 1 inverse agonist rimonabant inhibited the antiseizure activity of 2-LG, although it did not significantly affect T1117 fluorescence.Conclusion: These results suggest that 2-LG exerts an antiseizure effect through interactions between the 5-HT1A receptor and GPR55.","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":"36 17","pages":"1009-1015"},"PeriodicalIF":2.1,"publicationDate":"2025-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146010849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

PDK4 suppresses high glucose-induced microglial ferroptosis by restricting pro-ferroptotic PUFA biosynthesis. PDK4通过限制亲铁性PUFA生物合成来抑制高糖诱导的小胶质细胞铁下垂。

IF 1.7 4区医学

Neuroreport Pub Date : 2025-11-28 DOI: 10.1097/WNR.0000000000002234

Huahua Su, Zhihui Liu, Jiahao Wei, Ying Liu, Yuke Zhong, Xi Liu, Changhong Tan, Lifen Chen

{"title":"PDK4 suppresses high glucose-induced microglial ferroptosis by restricting pro-ferroptotic PUFA biosynthesis.","authors":"Huahua Su, Zhihui Liu, Jiahao Wei, Ying Liu, Yuke Zhong, Xi Liu, Changhong Tan, Lifen Chen","doi":"10.1097/WNR.0000000000002234","DOIUrl":"10.1097/WNR.0000000000002234","url":null,"abstract":"Background: Diabetes significantly elevates the risk of neurodegenerative disorders, including Alzheimer's disease and Parkinson's disease, indicating shared pathophysiological mechanisms. While ferroptosis is increasingly implicated in neurodegeneration, microglia - highly vulnerable to ferroptosis - may mediate this link. However, it remains unknown whether high glucose (HG) directly induces microglial ferroptosis.Methods: Using HG-treated BV2 microglia, we integrated multiomics profiling (RNA-seq and targeted lipidomics), functional assays, and genetic manipulation of pyruvate dehydrogenase kinase 4 (PDK4) to investigate its role in HG-associated ferroptosis.Results: HG-induced microglial ferroptosis, characterized by iron overload, elevated malondialdehyde and mitochondrial reactive oxygen species, glutathione peroxidase 4 (GPX4) downregulation, and mitochondrial damage, including loss of membrane potential and ultrastructural disintegration. This was accompanied by upregulated PDK4 expression. PDK4 overexpression attenuated ferroptosis by preserving GPX4, reducing lipid peroxidation, and maintaining mitochondrial integrity; these protective effects were reversed by n-6 polyunsaturated fatty acid (PUFA) supplementation. Conversely, PDK4 knockdown exacerbated ferroptosis via amplified n-6 PUFA synthesis and oxidative stress. Mechanistically, PDK4 acts as a metabolic gatekeeper by restricting acetyl-CoA availability for the synthesis of pro-ferroptotic PUFAs, thereby curtailing iron-dependent lipid peroxidation.Conclusion: PDK4 is a critical regulator of HG-induced microglial ferroptosis, thereby bridging hyperglycemia-induced metabolic dysfunction and neurodegeneration. Our findings nominate PDK4 as a promising therapeutic target for diabetes-linked neurodegenerative diseases.","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145669273","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Sustained acidosis suppresses persistent sodium currents to regulate the excitability of medullary dorsal horn neurons in rats. 持续酸中毒抑制持续钠电流调节大鼠髓背角神经元的兴奋性。

IF 1.7 4区医学

Neuroreport Pub Date : 2025-11-18 DOI: 10.1097/WNR.0000000000002233

Jin-Hwa Cho, Il-Sung Jang

{"title":"Sustained acidosis suppresses persistent sodium currents to regulate the excitability of medullary dorsal horn neurons in rats.","authors":"Jin-Hwa Cho, Il-Sung Jang","doi":"10.1097/WNR.0000000000002233","DOIUrl":"10.1097/WNR.0000000000002233","url":null,"abstract":"Objectives: Acid-sensing ion channels (ASICs) are rapidly inactivated following activation by acidic extracellular pH. Consequently, mechanisms beyond ASICs are likely involved in modulating neuronal excitability under sustained acidic conditions. Therefore, this study investigated the impact of sustained acidic pH on neuronal excitability.Methods: Membrane current and voltage changes induced by acidic pH were recorded from acutely isolated rat medullary dorsal horn neurons using the whole-cell patch-clamp technique.Results: The steady-state inactivation relationship for extracellular pH revealed that most ASICs were completely inactivated at pH ≤ 6.5. Acidic pH depolarized medullary dorsal horn neurons with high affinity (EC50 of pH 6.9), a process mediated by ASIC activation. Acidic pH (≤6.9) also generated instantaneous action potentials; however, they immediately disappeared owing to the inactivation of voltage-gated Na⁺ channels. Action potentials reemerged depending on pH level, even under sustained acidic conditions. This reappearance of action potentials correlated with the extent to which acidic pH inhibited the persistent Na⁺ current mediated by voltage-gated Na⁺ channels.Conclusion: These findings suggest that under pathological conditions characterized by sustained extracellular pH reduction, such as inflammation, a persistent Na⁺ current may serve as a sensor for modulating neuronal excitability in response to prolonged acidic pH levels.","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145669232","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Abnormal functional connectivity density in patients with obsessive-compulsive disorder. 强迫症患者的功能连接密度异常。

IF 1.7 4区医学

Neuroreport Pub Date : 2025-11-17 DOI: 10.1097/WNR.0000000000002232

Zihe Xu, Linglong Chen, Zhijun Luo, Yuanyuan Wang, Xingbo Suo, Feng Ouyang, Xuewen Lu, Xianjun Zeng, Maorong Hu

{"title":"Abnormal functional connectivity density in patients with obsessive-compulsive disorder.","authors":"Zihe Xu, Linglong Chen, Zhijun Luo, Yuanyuan Wang, Xingbo Suo, Feng Ouyang, Xuewen Lu, Xianjun Zeng, Maorong Hu","doi":"10.1097/WNR.0000000000002232","DOIUrl":"10.1097/WNR.0000000000002232","url":null,"abstract":"Objective: This study investigated abnormal short- and long-range functional connectivity density (FCD) and resting-state functional connectivity (rsFC) within and outside the cortico-striatal-thalamic (CST) loop in patients with obsessive-compulsive disorder (OCD).Methods: Ninety-two patients with OCD and 75 healthy controls underwent multimodal MRI. Clinical assessments included the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS), Beck Anxiety Inventory, and Beck Depression Inventory. Voxel-based FCD analysis explored local and distant nodal changes, followed by seed-based rsFC analysis and correlation with clinical variables.Results: Compared with healthy controls, patients with OCD showed decreased short-range FCD in the bilateral postcentral gyrus, left superior temporal gyrus, and right insula, but increased short-range FCD in the left caudate nucleus. Long-range FCD increased in the right orbitofrontal gyrus and left middle frontal gyrus. Seed-based analysis revealed enhanced rsFC between the right orbitofrontal gyrus and right calcarine fissure and surrounding cortex, and between the left middle frontal gyrus and right anterior cingulate and paracingulate gyri, as well as the right paracentral lobule. Left caudate FCD values negatively correlated with Y-BOCS scores, while left middle frontal gyrus FCD values positively correlated with illness duration.Conclusion: Patients with OCD exhibit widespread connectivity abnormalities in multiple brain regions within and beyond the classic CST loop, involving sensorimotor networks, emotion-cognitive regulation, executive control, error monitoring, and visual processing systems. These findings suggest that OCD pathophysiology extends beyond the traditional CST loop, providing new insights into the neural mechanisms underlying this disorder.","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145669257","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Sodium butyrate attenuates early brain injury and neuronal apoptosis after subarachnoid hemorrhage in rats via GPR41/PI3K/Akt pathway. 丁酸钠通过GPR41/PI3K/Akt通路减轻大鼠蛛网膜下腔出血后早期脑损伤和神经元凋亡。

IF 1.7 4区医学

Neuroreport Pub Date : 2025-11-10 DOI: 10.1097/WNR.0000000000002231

Chen Liang, Meiling Yu, Kang Liu, Yufei Ge

{"title":"Sodium butyrate attenuates early brain injury and neuronal apoptosis after subarachnoid hemorrhage in rats via GPR41/PI3K/Akt pathway.","authors":"Chen Liang, Meiling Yu, Kang Liu, Yufei Ge","doi":"10.1097/WNR.0000000000002231","DOIUrl":"10.1097/WNR.0000000000002231","url":null,"abstract":"Objective: Butyrate, a short-chain fatty acid produced by intestinal microbial fermentation of dietary fiber, serves as an endogenous ligand for the G protein-coupled receptors. Previous studies have confirmed the neuroprotective effects of sodium butyrate (NaB) in ischemic stroke, but its role in subarachnoid hemorrhage (SAH) remains unclear. Here, we investigated the potential therapeutic efficacy and underlying mechanisms of NaB in a rat SAH model.Methods: NaB was administered intranasally 1 h post-SAH, and neurological function and neuronal apoptosis were evaluated 24 h post-SAH.Results: During the early brain injury (EBI) phase after SAH, GPR41 was predominantly expressed in neuronal cells, and its expression levels increased significantly, peaking at 24 h post-SAH. NaB treatment attenuated neurological deficits after SAH, reduced brain edema, and alleviated neuronal damage and apoptosis. Furthermore, NaB elevated the levels of GPR41, phosphorylated Akt, and the antiapoptotic protein Bcl-2, while suppressing the expression of the proapoptotic protein Bax. Notably, the neuroprotective effects of NaB were partially reversed by GPR41 siRNA knockdown and pharmacological inhibition of PI3K with LY294002.Conclusions: These findings suggest that NaB may mitigate EBI after SAH by inhibiting neuronal apoptosis, with the underlying mechanism potentially involving activation of the GPR41/PI3K/Akt signaling pathway.","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145669279","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Zinc finger GATA-like protein 1 regulates apoptosis and phenotypic transformation via protein kinase B pathway in human vascular smooth muscle cells. 锌指gata样蛋白1通过蛋白激酶B途径调控人血管平滑肌细胞的凋亡和表型转化。

IF 2.1 4区医学

Neuroreport Pub Date : 2025-11-05 Epub Date: 2025-09-24 DOI: 10.1097/WNR.0000000000002217

Zhaobin Zeng, Hongquan Zhu, Renhui Yi, Haibin Wang, Huasheng Zhou, Shanggui Yuan, Jianguo Zhong, Zhihao Zhang

{"title":"Zinc finger GATA-like protein 1 regulates apoptosis and phenotypic transformation via protein kinase B pathway in human vascular smooth muscle cells.","authors":"Zhaobin Zeng, Hongquan Zhu, Renhui Yi, Haibin Wang, Huasheng Zhou, Shanggui Yuan, Jianguo Zhong, Zhihao Zhang","doi":"10.1097/WNR.0000000000002217","DOIUrl":"10.1097/WNR.0000000000002217","url":null,"abstract":"Purpose: Intracranial aneurysms represent the primary source of subarachnoid hemorrhage, ranking as the third most common cerebrovascular disorder after cerebral thrombosis and hypertension-related brain hemorrhage. As a member of the GATA family transcription factors, the role of zinc finger GATA-like protein 1 (ZGLP1) was unclear in intracranial aneurysm. In the present research, the specific effects of ZGLP1 on the proliferation and phenotypic transformation of human aerobic smooth muscle cells (HASMCs) were investigated.Methods: Cell counting kit 8 and colony formation assays were performed to detect the growth of HASMCs. Cell migration was confirmed using transwell and wound healing assays. The apoptosis was analyzed using flow cytometry.Finding: ZGLP1 knockdown inhibited the viability and colony formation ability of HASMCs. Importantly, ZGLP1 knockdown effectively promoted the apoptosis of HASMCs. The migration of HASMCs was remarkably inhibited by ZGLP1-specific small interfering RNA. Mechanistically, ZGLP1 knockdown inhibits the phosphorylation of protein kinase B (AKT) and cyclin D1 expression. In addition, ZGLP1 knockdown inhibited the expression of SMA and SM22α, while promoting the expression of OPN and MMP-2 in HASMCs, suggesting that ZGLP1 knockdown initiated the transformation from contractile phenotype to synthetic phenotype of HASMCs.Conclusion: ZGLP1 knockdown induces apoptosis through the AKT pathway, and also induces the phenotypic transformation of HASMCs. ZGLP1 is a potential therapeutic target for intracranial aneurysm and deserves further research.","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":"36 16","pages":"960-966"},"PeriodicalIF":2.1,"publicationDate":"2025-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145192158","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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