Acta neurobiologiae experimentalis最新文献

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Glymphatic system and aquaporin‑4 in epilepsy. 癫痫中的淋巴系统和水传导蛋白-4。
IF 1.4 4区 医学
Acta neurobiologiae experimentalis Pub Date : 2023-12-29 DOI: 10.55782/ane-2023-2498
Dorota Nowicka
{"title":"Glymphatic system and aquaporin‑4 in epilepsy.","authors":"Dorota Nowicka","doi":"10.55782/ane-2023-2498","DOIUrl":"10.55782/ane-2023-2498","url":null,"abstract":"<p><p>Over the past decade glymphatic concept has gained more and more interest. Despite some lacking data regarding structural and functional aspects, glymphatic system is widely considered the main mechanism of water and solutes transport in brain parenchyma, as well as waste clearance from the brain. Glymphatic system modulates the extracellular space volume and is involved in spatial K+ buffering (via influencing Kir4.1 channel functioning), two factors crucial for neuronal excitability and seizure susceptibility, and is itself strongly stimulated during sleep. This review summarizes information regarding the potential role of the glymphatic system in the development and progression of epilepsy, especially the role of the glial water channel aquaporin‑4 in modulation of brain excitability and in epilepsy. Data from animal models and human studies are presented.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 4","pages":"447-458"},"PeriodicalIF":1.4,"publicationDate":"2023-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139465819","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
Pylabianca: comprehensive and user‑friendly Python package for single‑neuron data analysis. Pylabianca:用于单神经元数据分析的全面且用户友好的 Python 软件包。
IF 1.4 4区 医学
Acta neurobiologiae experimentalis Pub Date : 2023-12-28 DOI: 10.55782/ane-2023-2440
Mikołaj Magnuski, Władysław Średniawa, Katarzyna Paluch, Davor Ivanovski, Harish Babu, Jan Kaminski
{"title":"Pylabianca: comprehensive and user‑friendly Python package for single‑neuron data analysis.","authors":"Mikołaj Magnuski, Władysław Średniawa, Katarzyna Paluch, Davor Ivanovski, Harish Babu, Jan Kaminski","doi":"10.55782/ane-2023-2440","DOIUrl":"10.55782/ane-2023-2440","url":null,"abstract":"<p><p>In the area of electrophysiology, the availability of comprehensive and user‑friendly tools for single-neuron data processing, statistical analysis, and fast, intuitive data visualization is limited. To address this gap, we introduce pylabianca, a Python library tailored for robust single and multi‑unit data processing. Pylabianca leverages the power of standard Python packages and adopts the application programming interface of MNE‑Python, one of the most widely used electrophysiology packages. One of pylabianca's primary objectives is to provide a low entry threshold for scientists, requiring only basic Python programming skills. Pylabianca was designed to streamline most common analyses of single neuron data, and provide convenient data structures to serve as a foundation for building custom analysis pipelines. We believe that pylabianca will contribute to enhancing researchers' capabilities and efficiency in the field of single-neuron electrophysiology.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 4","pages":"432-446"},"PeriodicalIF":1.4,"publicationDate":"2023-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139465824","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
Molecular mechanisms and treatment strategies for methamphetamine‑induced neurodegeneration, inflammation and neurotoxicity. 甲基苯丙胺诱导的神经变性、炎症和神经毒性的分子机制和治疗策略。
IF 1.4 4区 医学
Acta neurobiologiae experimentalis Pub Date : 2023-12-28 DOI: 10.55782/ane-2023-2488
Samareh Omidvari, Zahra Azimzadeh, Fariborz Rashnoo, Foozhan Tahmasebinia, Aliasghar Keramatinia, Navid Ahmady Roozbahany, Hojjat Allah Abbaszadeh, Shahram Darabi
{"title":"Molecular mechanisms and treatment strategies for methamphetamine‑induced neurodegeneration, inflammation and neurotoxicity.","authors":"Samareh Omidvari, Zahra Azimzadeh, Fariborz Rashnoo, Foozhan Tahmasebinia, Aliasghar Keramatinia, Navid Ahmady Roozbahany, Hojjat Allah Abbaszadeh, Shahram Darabi","doi":"10.55782/ane-2023-2488","DOIUrl":"10.55782/ane-2023-2488","url":null,"abstract":"<p><p>Methamphetamine (METH) is a highly addictive psychostimulant known for its profound impact on the nervous system. Chronic METH use leads to neurotoxicity characterized by various molecular and structural alterations in the brain. This review article primarily aims to elucidate the mechanisms underlying METH‑induced neurotoxicity. METH's mechanism of action involves the inhibition of dopamine, serotonin, and norepinephrine reuptake, resulting in altered synaptic function. Prolonged METH exposure triggers oxidative stress, endoplasmic reticulum stress, mitochondrial dysfunction, impaired axonal transport, autophagy, and programmed cell death, ultimately contributing to neurotoxicity. These neurotoxic effects manifest as increased neuronal firing rate, disruptions in intracellular ion balance (Ca2+ and Na+), energy production imbalances, and excessive reactive oxygen species production. The blood‑brain barrier is compromised, leading to structural, functional, and neurochemical alterations, particularly in the fronto‑striatal circuit. While our comprehensive review addresses these intricate molecular and structural changes induced by METH, we also examined the latest therapeutic strategies designed to mitigate neurotoxicity. Our investigation sheds light on the critical need to comprehend the complex pathways underlying METH‑induced neurotoxicity and develop effective treatment approaches.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 4","pages":"414-431"},"PeriodicalIF":1.4,"publicationDate":"2023-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139465822","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
Early development of the Tsc1 Purkinje cell specific mouse knockouts. Tsc1浦肯野细胞特异性基因敲除小鼠的早期发育。
IF 1.4 4区 医学
Acta neurobiologiae experimentalis Pub Date : 2023-12-12 DOI: 10.55782/ane-2023-2472
Anna Sługocka, Marta Anna Przybyła, Jarosław Jerzy Barski
{"title":"Early development of the Tsc1 Purkinje cell specific mouse knockouts.","authors":"Anna Sługocka, Marta Anna Przybyła, Jarosław Jerzy Barski","doi":"10.55782/ane-2023-2472","DOIUrl":"10.55782/ane-2023-2472","url":null,"abstract":"<p><p>Tsc1 is a gene which expression results in hamartin, a protein involved in regulation of the mTOR1 pathway. Inactivation of Tsc1 gives rise to hyperactivation of the mTOR1 machinery, increased proliferation and growth of cells with subsequent cell degeneration and cell death. In humans, mutations of Tsc1 result in an inherited disorder ‑ tuberous sclerosis complex (TSC) with the concomitant multiorgan non‑malignant tumors (tubers), epileptic seizures and autistic‑like manifestations. General mouse knock‑outs, homozygous for the inactivated Tsc1 alleles do not survive and die at early embryonal stages. To circumvent this problem, we utilized the Cre/loxP system and removed Tsc1 specifically in Purkinje cells using the pcp2/L7Cre mouse strain and the Tsc1tmDjk/J strains. Because of the published results showing the autistic‑like symptoms after the same crossbred, we have decided to look closer at the early postnatal period of these mutants. Surprisingly no evidence of any behavioral alterations were found, including the ultrasonic vocalizations of newborns. We decided to focus more attention on the interpretation of data, including a more detailed statistical evaluation of our results.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 4","pages":"404-413"},"PeriodicalIF":1.4,"publicationDate":"2023-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139465794","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
Effect of low‑frequency repetitive transcranial magnetic stimulation on cognitive function in rats with medial temporal lobe epilepsy. 低频重复经颅磁刺激对内侧颞叶癫痫大鼠认知功能的影响
IF 1.4 4区 医学
Acta neurobiologiae experimentalis Pub Date : 2023-12-11 DOI: 10.55782/ane-2023-2471
Li-Qin Che, Zhen-Zhen Qu, Tao Xie, Yan-Ge Zhang, Dong-Juan Yuan, Qing Li, Li-Jing Jia, Wei-Ping Wang
{"title":"Effect of low‑frequency repetitive transcranial magnetic stimulation on cognitive function in rats with medial temporal lobe epilepsy.","authors":"Li-Qin Che, Zhen-Zhen Qu, Tao Xie, Yan-Ge Zhang, Dong-Juan Yuan, Qing Li, Li-Jing Jia, Wei-Ping Wang","doi":"10.55782/ane-2023-2471","DOIUrl":"10.55782/ane-2023-2471","url":null,"abstract":"<p><p>Epilepsy, especially the medial temporal lobe epilepsy (TLE), can result in cognitive impairment. Low‑frequency repetitive magnetic stimulation (rTMS) has been verified to suppress neural excitability and reduce seizures. Given its potential in modifying cortical activity, we aimed to investigate its impact on cognitive function in the context of epilepsy, a condition where the use of rTMS has not been extensively explored. However, the influence on cognitive function has not yet been investigated. Therefore, this study aimed to investigate the effects of low‑frequency rTMS on cognitive improvement in epileptic rats. Rats used in this study were randomly divided into five groups: the sham group, the epilepsy group, and three epilepsy groups treated with rTMS at different frequencies. Each group underwent the Morris water maze test to investigate hippocampus‑dependent episodic memory, to evaluate their cognitive performance. Further assessments included patch clamp and western blot techniques to estimate the synaptic function in the hippocampus. Comparison between groups showed that low‑frequency rTMS significantly reduced spontaneous recurrent seizures and improved spatial learning and memory impairment in epileptic rats. Additionally, rTMS remodeled the synaptic plasticity affected by seizures and notably enhanced the expression of AMPAR and synaptophysin. Low‑frequency rTMS can antagonize the cognitive impairment caused by TLE, and promote synaptic connections.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 4","pages":"395-403"},"PeriodicalIF":1.4,"publicationDate":"2023-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139465816","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
Systematic review and meta‑analysis of observational studies to check the protective role of non‑steroidal anti‑inflammatory drugs in Alzheimer's disease. 对观察性研究进行系统回顾和荟萃分析,检查非甾体抗炎药对阿尔茨海默病的保护作用。
IF 1.4 4区 医学
Acta neurobiologiae experimentalis Pub Date : 2023-12-04 DOI: 10.55782/ane-2023-2467
Akash Asthana, Shashank Tripathi, Rachna Agarwal
{"title":"Systematic review and meta‑analysis of observational studies to check the protective role of non‑steroidal anti‑inflammatory drugs in Alzheimer's disease.","authors":"Akash Asthana, Shashank Tripathi, Rachna Agarwal","doi":"10.55782/ane-2023-2467","DOIUrl":"10.55782/ane-2023-2467","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a major neurodegenerative disease, affecting more than two third cases of dementia in the world. Non‑steroidal anti‑inflammatory drugs (NSAIDs) are widely used anti‑inflammatory analgesic agents representing 7.7% of worldwide prescriptions of which 90% are in patients over 65 years old. Based on mixed findings a systematic review and meta‑analysis were conducted to develop a better understanding of the protective role of NSAIDs in AD. We used three database PubMed, Web of Science, and Embase to identify the literatures. The studies following cohort and case‑control design were investigated separately to check the effect of NSAIDs on AD, by the using their fundamental indicators (relative risk and odds ratio). The fixed effect or random effects model were used to estimate the pooled relative risk and pooled odds ratio separately for both the study design, based on magnitude of heterogeneity. A total of 14 studies were selected for meta‑analysis. Eight studies were following cohort study design, whereas, six studies were following case‑control study design. In meta‑analysis of cohort studies, the pooled relative risk was 0.67 with 95% C.I 0.39 to 1.15, which was statistically insignificant. In meta‑analysis of case‑control studies, the pooled odds ratio was 0.71 with 95% C.I 0.46 to 1.10, which was statistically insignificant. NSAIDs do not act as a protective factor for Alzheimer's disease. Additionally, methodologically sound randomized controlled trials are required to produce a robust result.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 4","pages":"386-394"},"PeriodicalIF":1.4,"publicationDate":"2023-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139465827","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
The protective role of circ_0016760 downregulation against sevoflurane‑induced neurological impairment via modulating miR‑145 expression in aged rats. 通过调节 miR-145 的表达下调 circ_0016760 对七氟烷诱导的老年大鼠神经损伤的保护作用
IF 1.4 4区 医学
Acta neurobiologiae experimentalis Pub Date : 2023-12-01 DOI: 10.55782/ane-2023-2464
Peiyu Shuai, Zhihong Hu, Wei Li, Guoliang You, Zhiye Liu, Niandong Zheng
{"title":"The protective role of circ_0016760 downregulation against sevoflurane‑induced neurological impairment via modulating miR‑145 expression in aged rats.","authors":"Peiyu Shuai, Zhihong Hu, Wei Li, Guoliang You, Zhiye Liu, Niandong Zheng","doi":"10.55782/ane-2023-2464","DOIUrl":"10.55782/ane-2023-2464","url":null,"abstract":"<p><p>Sevoflurane can produce toxicity to the hippocampal tissues of brain, leading to nerve damage, causing learning and cognitive dysfunction. CircRNAs have been indicated to act as a key mediator in anesthetic neurotoxicity. This study focused on the effect of circ_0016760 on sevoflurane‑induced neurological impairment. The GEO database (GSE147277) and RT‑qPCR were used to predict and  measure the circ_0016760 expression. The interaction of circ_0016760 and miR‑145 was verified by dual‑luciferase reporter assay. The CCK‑8 assay, flow cytometry, ELISA, ROS kit, MWM test were carried out to measure the cell viability, apoptosis, inflammation indicators, ROS level, and cognitive and memory function of the rats. Sevoflurane exacerbated neurotoxicity by restraining cell viability, inducing cell apoptosis, neuroinflammation, and ROS generation, and causing learning and cognitive dysfunction. Circ_0016760 expression was increased in POCD patients from the GEO database and upregulated after sevoflurane exposure. miR‑145 was a target miRNA of circ_0016760. Silencing of circ_0016760 weakened the effect of sevoflurane on cell viability, cell apoptosis, inflammation‑related factors, oxidative stress, which could be reversed by miR‑145 inhibitor. The animal experiments results showed that circ_0016760 played a protective effect on regulating the cognitive behavior of sevoflurane‑treated aged rats, expression of inflammation cytokine, and oxidative stress factors through targeting miR‑145 in sevoflurane‑treated aged rat's hippocampal neurons. Our results revealed that silencing of circ_0016760 attenuated sevoflurane‑induced hippocampal neuron injury by regulating miR‑145 expression, which may provide potential insights into the treatment of sevoflurane‑induced neurological impairment.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 4","pages":"377-385"},"PeriodicalIF":1.4,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139465833","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
The less complex temporal patterns of resting‑state EEG activity, the lower the visual temporal order threshold. 静息态脑电图活动的时间模式越不复杂,视觉时序阈值就越低。
IF 1.4 4区 医学
Acta neurobiologiae experimentalis Pub Date : 2023-11-30 DOI: 10.55782/ane-2023-2463
Monika Lewandowska, Krzysztof Tołpa, Marcin Hajnowski, Tomasz Piotrowski, Joanna Dreszer
{"title":"The less complex temporal patterns of resting‑state EEG activity, the lower the visual temporal order threshold.","authors":"Monika Lewandowska, Krzysztof Tołpa, Marcin Hajnowski, Tomasz Piotrowski, Joanna Dreszer","doi":"10.55782/ane-2023-2463","DOIUrl":"10.55782/ane-2023-2463","url":null,"abstract":"<p><p>Speech understanding, watching a movie, listening to music etc., requires perception of the temporal order of at least two incoming events. A history of performing these tasks may be reflected in spontaneous brain activity. Here, we examined the relationship between the complexity (temporal dynamics) of resting‑state EEG (rsEEG) signal, assessed using the multivariate MultiScale Entropy (mMSE) algorithm, and the perception of event ordering, indexed by a visual temporal order threshold (TOT), i.e., the minimum duration necessary to correctly identify the before‑after relation between two stimuli. Healthy adolescents and young adults performed a psychophysical task measuring the TOT and underwent an eyes‑closed rsEEG study. The features of mMSE vectors, namely the area under curve (AUC) that represents total signal complexity, as well as the MaxSlope and the AvgEnt, corresponding to the entropy at fine‑ and coarse‑grained timescales, respectively, were obtained for the central (midline), anterior, middle and posterior channel sets. The greater the AUC and AvgEnt values in the central, left and right posterior areas, and the higher AUC in the right middle region, the higher the TOT. The most significant relationships were found for the midline electrodes (Fz, Cz, Pz, Oz). There were no significant correlations between the MaxSlope values and the TOT. To the best of our knowledge, this is the first study demonstrating that spontaneous EEG signal complexity is associated with the temporal order perception of two stimuli presented in rapid succession. Our findings may indicate that low total and coarse entropy levels of rsEEG signal are beneficial for visual temporal order judgments.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 4","pages":"359-376"},"PeriodicalIF":1.4,"publicationDate":"2023-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139465830","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
Dendritic arbor dynamics and stability in health and disease. 树突树轴在健康和疾病中的动态和稳定性
IF 1.4 4区 医学
Acta neurobiologiae experimentalis Pub Date : 2023-11-22 DOI: 10.55782/ane-2023-2456
Magdalena Mlostek, Juan Zeng, Malgorzata Urbanska, Jacek Jaworski
{"title":"Dendritic arbor dynamics and stability in health and disease.","authors":"Magdalena Mlostek, Juan Zeng, Malgorzata Urbanska, Jacek Jaworski","doi":"10.55782/ane-2023-2456","DOIUrl":"10.55782/ane-2023-2456","url":null,"abstract":"<p><p>Dendritogenesis, a process of dendritic arbor development, is essential for the formation of functional neuronal networks, and in mammals, it begins in early life and continues into adulthood. It is a highly dynamic process in which dendritic branches form and regress until mature connectivity is achieved. Thereafter, dendritic branches are considered stable and do not undergo substantial rearrangements, although several exceptions have been described in the literature. After this long period of relative stability, significant changes in dendritic branching occur when the brain begins to age. Several neurological diseases, occurring both during development and in adulthood, have severe effects on the morphology of dendritic arbors, often associated with intellectual dysfunction. The molecular mechanisms of dendritogenesis are fairly well described. In contrast, knowledge of the molecular mechanisms of dendritic arbor stabilization and pathology‑induced instability is still quite incomplete, and several important questions remain unanswered. We describe the dynamic changes during development and adulthood and in different pathologies. Whenever possible, we also provide details on the molecular mechanisms behind dendritic dynamics and stability.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 4","pages":"331-358"},"PeriodicalIF":1.4,"publicationDate":"2023-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139465792","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
IL‑4 alleviates CIRI by suppressing autophagy via the HIF‑1α/Bcl‑2/BNIP3 pathway in rats. IL‑4通过HIF-1α/Bcl‑2/BNIP3途径抑制大鼠自噬,从而减轻CIRI。
IF 1.4 4区 医学
Acta neurobiologiae experimentalis Pub Date : 2023-09-29 DOI: 10.55782/ane-2023-2429
Yijun Suo, Lu Zhang, Yuanhang Che
{"title":"IL‑4 alleviates CIRI by suppressing autophagy via the HIF‑1α/Bcl‑2/BNIP3 pathway in rats.","authors":"Yijun Suo,&nbsp;Lu Zhang,&nbsp;Yuanhang Che","doi":"10.55782/ane-2023-2429","DOIUrl":"10.55782/ane-2023-2429","url":null,"abstract":"<p><p>This paper was designed for delving into the mechanism adopted by interleukin‑4 (IL‑4) to relieve cerebral ischemia‑reperfusion injury (CIRI) in rats via suppressing autophagy. Herein, rats stochastically fell into sham operation (sham), model (RI), model + IL‑4 intervention (IL‑4), model + HIF‑1α inhibitor (2‑methoxyestradiol, 2ME2) and model + IL‑4 + 2ME2 (IL‑4 + 2ME2) groups. Next, western blotting was utilized to examine the protein expressions of microtubule‑associated protein 1 light chain 3 (LC3), p62, hypoxia‑inducible factor 1‑alpha (HIF‑1α) and Bcl‑2/adenovirus E1B 19 kDa‑interacting protein 3 (BNIP3). Relative to RI group, IL‑4 group had a significantly lower neurological impairment scale (NIS) score and an overtly lower apoptosis rate of neurons as well as a strikingly smaller cerebral infarction volume and number of autophagosomes (P<0.05). The LC3II/LC3I ratio and HIF‑1α and BNIP3 protein expressions dropped, but p62 protein expression rose pronouncedly in IL‑4 group (P<0.05). In contrast to those in RI group, the NIS score, neuronal apoptosis rate, cerebral infarction volume and autophagosome number were strikingly reduced (P<0.05). The NIS score, cerebral infarction volume, neuronal apoptosis rate, autophagosome number, LC3II/LC3I ratio and protein expressions of HIF‑1α and BNIP3 plummeted, while p62 protein expression sharply rose in IL‑4 + 2ME2 group relative to those in IL‑4 group (P<0.05). IL‑4 suppresses cell autophagy by inhibiting the HIF‑1α/BNIP3 pathway, thus relieving CIRI in rats.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 3","pages":"246-254"},"PeriodicalIF":1.4,"publicationDate":"2023-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49688305","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
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