IBRO Neuroscience Reports最新文献

{"title":"Spontaneous running wheel exercise during pregnancy prevents later neonatal-anoxia-induced somatic and neurodevelopmental alterations","authors":"","doi":"10.1016/j.ibneur.2024.08.008","DOIUrl":"10.1016/j.ibneur.2024.08.008","url":null,"abstract":"<div><h3>Introduction</h3><p>About 15–20 % of babies that suffer perinatal asphyxia die and around 25 % of the survivors exhibit permanent neural outcomes. Minimization of this global health problem has been warranted. This study investigated if the offspring of pregnant female rats allowed to spontaneously exercise on running wheels along a 11-day pregnancy period were protected for somatic and neurodevelopmental disturbs that usually follow neonatal anoxia.</p></div><div><h3>Methods</h3><p>spontaneous exercise was applied to female rats which were housed in cages allowing free access to running wheels along a 11-day pregnancy period. Their offspring were submitted to anoxia 24–36 h after birth. Somatic and sensory-motor development of the pups were recorded until postnatal day 21 (P21). Myelin basic protein (MBP)-stained areas of sensory and motor cortices were measured at P21. Neuronal nuclei (NeuN)-immunopositive cells and synapsin-I levels in hippocampal formation were estimated at P21 and P75.</p></div><div><h3>Results</h3><p>gestational exercise and / or neonatal anoxia increased the weight and the size of the pups. In addition, gestational exercise accelerated somatic and sensory-motor development of the pups and protected them against neonatal-anoxia-induced delay in development. Further, neonatal anoxia reduced MBP stained area in the secondary motor cortex and decreased hippocampal neuronal estimates and synapsin-I levels at P21; gestational exercise prevented these effects. Therefore, spontaneous exercise along pregnancy is a valuable strategy to prevent neonatal-anoxia-induced disturbs in the offspring.</p></div><div><h3>Conclusion</h3><p>spontaneous gestational running wheel exercise protects against neonatal anoxia-induced disturbs in the offspring, including (1) physical and neurobehavioral developmental impairments, and (2) hippocampal and cortical changes. Thus, spontaneous exercise during pregnancy may represent a valuable strategy to prevent disturbs which usually follow neonatal anoxia.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2024-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242124000770/pdfft?md5=c7138664cf6f01fd9fbb8b156b21d778&pid=1-s2.0-S2667242124000770-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142162654","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cannabinoid type 2 receptor deficiency leads to Aβ-induced cognitive impairment through promoting microglial sensitivity to Aβ in the prefrontal cortex in mice","authors":"","doi":"10.1016/j.ibneur.2024.08.004","DOIUrl":"10.1016/j.ibneur.2024.08.004","url":null,"abstract":"<div><h3>Aims</h3><p>This study is to investigate the effects of Cannabinoid type 2 receptor (CB₂R) deficiency on microglia and cognitive function in both Aβ_1–42-injected CB₂R knockout mice and a transgenic mouse model of Alzheimer’s disease (AD) in brain.</p></div><div><h3>Methods</h3><p>After hippocampal injection with Aβ_1–42 oligomers in CB₂R knockout mice with and without CB₂R agonist treatment and in transgenic APP/PS1 mice with CB₂R deletion, the novel object recognition (NOR) and Morris water maze (MWM) tests were performed to assess the animal behavior performance. Immunofluorescence staining was conducted to detect the microglial morphology and activation status. The expression of proinflammation and anti-inflammation cytokines were determined by qRT-PCR.</p></div><div><h3>Results</h3><p>CB₂R deficiency significantly aggravated cognitive impairment in both Aβ_1–42-induced and transgenic APP/PS1 animal model in NOR. In Aβ-injected mice lacking CB₂R and transgenic APP/PS1 mice with CB₂R deletion, microglia in the prefrontal cortex exhibited enhanced immunoreactivity with altered morphology. Furthermore, transformation of activated microglial phenotype in the prefrontal cortex was reduced in Aβ_1–42-injected CB₂R knockout mice after CB₂R agonist treatment. The CB₂R deficiency significantly increased the expression of proinflammatory cytokines in the prefrontal cortex, while it was observed in the hippocampus in both Aβ_1–42-injected and transgenic APP/PS1 AD mouse model. Furthermore, CB₂R deficiency increased concentrations of soluble Aβ ₄₀ in the prefrontal cortex, but did not affect plaques deposition.</p></div><div><h3>Conclusion</h3><p>CB₂R deletion led to enhanced neuroinflammatory responses via direct upregulating microglia activation in the prefrontal cortex during the early symptomatic phase of AD mice. CB₂R modulates prefrontal cortical neuroinflammation, which is essential for regulating cognitive functions such as recognition memory at the early stage of AD.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242124000745/pdfft?md5=808ebd9fab4377faf70cc0b1061aec36&pid=1-s2.0-S2667242124000745-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142150927","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of microwave radiation on adult neurogenesis and behavior of prenatally exposed rats","authors":"","doi":"10.1016/j.ibneur.2024.08.007","DOIUrl":"10.1016/j.ibneur.2024.08.007","url":null,"abstract":"<div><p>Postnatal neurogenesis appears to be highly sensitive to environmental factors, including microwave electromagnetic radiation (MWR). Here, we investigated the impact of MWR during intrauterine development on juvenile and adult neurogenesis in the rostral migratory stream (RMS) and the dentate gyrus of the hippocampus in the rat brain, as well as its effect on animal behavior. Female rats were exposed to MWR at a frequency of 2.45 GHz for 2 hours daily throughout pregnancy. The offspring of irradiated mothers survived to either juvenile age or adulthood. The brains of the rats were subjected to morphological analysis, assessing cell proliferation and death in both neurogenic regions. In the RMS, the differentiation of nitrergic neurons was also investigated. The effect of MWR on behavior was evaluated in rats surviving to adulthood. Prenatal MWR exposure caused significant changes in the number of proliferating and dying cells, depending on the age of the animals and the observed neurogenic region. In addition, MWR attenuated the maturation of nitrergic neurons in the RMS in both juvenile and adult rats. Morphological alterations in neurogenesis were accompanied by changes in animals’ behavior. Affected neurogenesis and changes in animal behavior suggest a high sensitivity of the developing brain to MWR.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2024-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242124000782/pdfft?md5=1f16384ea2b024f7a34ebfb9afd9ced8&pid=1-s2.0-S2667242124000782-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142136894","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modulation of CB1 cannabinoid receptor alters the electrophysiological properties of cerebellar Purkinje cells in harmaline-induced essential tremor","authors":"","doi":"10.1016/j.ibneur.2024.08.005","DOIUrl":"10.1016/j.ibneur.2024.08.005","url":null,"abstract":"<div><p>Essential tremor (ET) is one of the most common motor disorders with debilitating effects on the affected individuals. The endocannabinoid system is widely involved in cerebellar signaling. Therefore, modulation of cannabinoid-1 receptors (CB1Rs) has emerged as a novel target for motor disorders. In this study, we aimed to assess whether modulation of cannabinoid receptors (CBRs) could alter the electrophysiological properties of Purkinje cells (PCs) in the harmaline-induced ET model. Male Wistar rats were assigned to control, harmaline (30 mg/kg), CBR agonist WIN 55,212–2 (WIN; 1 mg/kg), CB1R antagonists AM251 (1 mg/kg) and rimonabant (10 mg/kg). Spontaneous activity and positive and negative evoked potentials of PCs were evaluated using whole-cell patch clamp recording. Findings demonstrated that harmaline exposure induced alterations in the spontaneous and evoked firing behavior of PCs, as evidenced by a significant decrease in the mean number of spikes and half-width of action potential in spontaneous activity. WIN administration exacerbated the electrophysiological function of PCs, particularly in the spontaneous activity of PCs. However, CB1R antagonists provided protective effects against harmaline-induced electrophysiological changes in the spontaneous activity of PCs. Our findings reinforce the pivotal role of the endocannabinoid system in the underlying electrophysiological mechanisms of cerebellar disorders and suggest that antagonism of CB1R might provide therapeutic utility.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242124000757/pdfft?md5=3abe388053f012b412fd994055d69840&pid=1-s2.0-S2667242124000757-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142044365","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Celastrol alleviates secondary brain injury following intracerebral haemorrhage by inhibiting neuronal ferroptosis and blocking blood-brain barrier disruption","authors":"","doi":"10.1016/j.ibneur.2024.08.003","DOIUrl":"10.1016/j.ibneur.2024.08.003","url":null,"abstract":"<div><h3>Background</h3><p>Following recent research advancements, an increasing level of evidence had been published to indicate that celastrol exerted a therapeutic effect on a range of nervous system diseases. This study therefore aimed to investigate the potential involvement of celastrol on ferroptosis and the blood-brain barrier disruption in intracerebral haemorrhage.</p></div><div><h3>Methods</h3><p>We established a rat intracerebral haemorrhage and adrenal pheochromocytoma cell (PC12) OxyHb models using an ACSL4 overexpression vector. Ferroptosis-related indices were assessed using corresponding assay kits, and immunofluorescence and flow cytometry were used to measure reactive oxygen species (ROS) levels. Additionally, quantitative PCR (qPCR) and western blot analyses were conducted to evaluate the expression of key proteins and elucidate the role of celastrol in intracerebral haemorrhage (ICH).</p></div><div><h3>Results</h3><p>Celastrol significantly improved neurological function scores, blood-brain barrier integrity, and brain water content in rats with ICH. Moreover, subsequent analysis of ferroptosis-related markers, such as Fe2+, ROS, MDA, and SOD, suggested that celastrol exerted a protective effect against the oxidative damage induced by ferroptosis in ICH rats and cells. Furthermore, Western blotting indicated that celastrol attenuated ferroptosis by modulating the expression levels of key proteins, including acyl-CoA synthetase long-chain family member 4 (ACSL4), glutathione peroxidase 4 (GPX4), ferritin heavy chain 1 (FTH1), and anti-transferrin receptor 1 (TFR1) both in vitro and in vivo. ACSL4 overexpression attenuated the neuroprotective effects of celastrol on ICH in vitro. Molecular docking analysis revealed that celastrol interacted with ACSL4 via the GLU107, GLN109, ASN111, and LYS357 binding sites.</p></div><div><h3>Conclusions</h3><p>Celastrol exerted antioxidant properties and aids in neurological recovery after stroke by suppressing ACSL4 expression during ferroptosis. As such, this drug represented a promising pharmaceutical candidate for the treatment of ICH.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2024-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242124000733/pdfft?md5=b58b04cfa9e8270a4cdf5448f845e38f&pid=1-s2.0-S2667242124000733-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141952846","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mapping the effect of the antisecretory factor on GABAA receptor α1 and α6 subunits in cerebellar granule cells in vitro","authors":"","doi":"10.1016/j.ibneur.2024.08.001","DOIUrl":"10.1016/j.ibneur.2024.08.001","url":null,"abstract":"<div><p>The Antisecretory Factor (AF) is a protein that can reduce intestinal hypersecretion and various inflammation disorders <em>in vivo</em>. Discovered in many mammalian tissues and plasma, its mechanism of action remains unknown. Interestingly, its induction has been found to counteract vertigo in patients with Méniere's disease. This suggests an inherent ability to control body balance and posture, an activity that may play a role in cerebellar function. Therefore, it may be worthwhile to investigate whether this activity can inhibit neuronal cells involved in cerebellar circuitries and its potential action on enteric nervous system ganglia, which could explain its antisecretory effect in the intestine.</p><p>Previously, we studied the role of AF on GABA_A receptors in cerebellar granule cells, taking advantage of electrophysiology and evaluating the effects of the administration of AF-16, an AF peptide. Treatment with AF-16 increased GABA_A receptor responses, especially those containing the α₆ subunit. Here, we performed immunofluorescence experiments by staining α₁ and α₆ subunits before and after incubation with AF-16, analyzed super-resolved images comparing pre- and post-treatment maps and critically examined these experimental results with our previous electrophysiological data to shed light on the mechanisms of action of AF protein on GABA_A receptor subpopulations, specifically the \"fast\" receptors of α_n β_2/3 γ₂ composition that contain either the α₁ or the α₆ subunit.</p><p>The results indicate that the α₆ subunit is redistributed, with a decrease in neurites and an increase in soma. Conversely, the α₁ subunit shows opposite results, with an increase in neurites and a decrease in soma.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2024-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242124000721/pdfft?md5=731aa284e890c83420f997f2645bbcd6&pid=1-s2.0-S2667242124000721-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141979140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chemokines play a role in nerve damage and neuroprotection in vascular dementia","authors":"","doi":"10.1016/j.ibneur.2024.08.002","DOIUrl":"10.1016/j.ibneur.2024.08.002","url":null,"abstract":"<div><p>Various Chemotactic Factors (FCs) play different roles in neuronal injury in vascular dementia. CXCL5 and CCL11 exacerbate neurological injury by promoting inflammatory responses. CXCL12/SDF-1 and CX3CL1 play neuroprotective roles.CXCL13, XCL-1 and CCL2/ MCP-1 exacerbate neurological injury in the early stage, while exerting neuronal regeneration and neuroprotective effects in the chronic progressive phase. Chemokines often play an important role in the course of vascular dementia by regulating inflammatory responses, oxidative stress, and autophagy. Activation of microglia plays an important role in the regression of vascular dementia. Activated microglia M1 causes neuronal damage through the release of chemokines. And microglia M2 has anti-inflammatory effects and is involved in the repair of brain damage. Therefore, dynamic monitoring of various related FCs and understanding the relationship between FCs and microglia can help to understand and regulate the disease course progression of vascular dementia.At present, many scholars have confirmed in basic research that different subgroups of chemokines are closely related to vascular dementia. In clinical research, new immunotherapy methods that upregulate XCL-1 and drugs that regulate the activity of CCL2/CCR2 signaling pathways are being studied and promoted.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2024-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S266724212400071X/pdfft?md5=2621e83bf9c81622baca20a8e1305936&pid=1-s2.0-S266724212400071X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141952845","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IL-33 relieves nerve injury by mediating microglial polarization in neuromyelitis optica spectrum disorders via the IL-33/ST2 pathway","authors":"","doi":"10.1016/j.ibneur.2024.07.008","DOIUrl":"10.1016/j.ibneur.2024.07.008","url":null,"abstract":"<div><p>Interleukin-33 (IL-33) is a member of the interleukin-1 cytokine family. Its function in regulating microglial M1/M2 polarization in neuromyelitis optica spectrum disorder (NMOSD) is still unelucidated. To evaluate the role of IL-33 in NMOSD, we constructed NMOSD mice model by injecting purified serum IgG from AQP4-IgG seropositive NMOSD patients into experimental autoimmune encephalomyelitis (EAE) mice, and IL-33 was intraperitoneally injected into NMOSD mice 3 d before the model induction. We found that pretreatment of the NMOSD mice with IL-33 relieved brain neuron loss, and demyelination and improved the structure of axons, astrocytes, and mitochondria. In the neuronal and microglial coculture system, pretreatment with IL-33 in microglia alleviated NMOSD serum-induced inflammation and damaged morphology in cultured neurons. IL-33 transformed microglia to the M2 phenotype, and NMOSD serum promoted microglia to the M1 phenotype in cultured BV2 cells. Moreover, IL-33 influenced microglial polarity via the IL-33/ST2 pathway. IL-33 may be a novel insight useful for further developing NMOSD-targeted therapy and drug development.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2024-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242124000708/pdfft?md5=f227b6420c787bafa3e0955d021cd661&pid=1-s2.0-S2667242124000708-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141952547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bipolar disorder: Construction and analysis of a joint diagnostic model using random forest and feedforward neural networks","authors":"","doi":"10.1016/j.ibneur.2024.07.007","DOIUrl":"10.1016/j.ibneur.2024.07.007","url":null,"abstract":"<div><h3>Background</h3><p>To construct a diagnostic model for Bipolar Disorder (BD) depressive phase using peripheral tissue RNA data from patients and combining Random Forest with Feedforward Neural Network methods.</p></div><div><h3>Methods</h3><p>Datasets GSE23848, GSE39653, and GSE69486 were selected, and differential gene expression analysis was conducted using the limma package in R. Key genes from the differentially expressed genes were identified using the Random Forest method. These key genes' expression levels in each sample were used to train a Feedforward Neural Network model. Techniques like L1 regularization, early stopping, and dropout layers were employed to prevent model overfitting. Model performance was then validated, followed by GO, KEGG, and protein-protein interaction network analyses.</p></div><div><h3>Results</h3><p>The final model was a Feedforward Neural Network with two hidden layers and two dropout layers, comprising 2345 trainable parameters. Model performance on the validation set, assessed through 1000 bootstrap resampling iterations, demonstrated a specificity of 0.769 (95 % CI 0.571–1.000), sensitivity of 0.818 (95 % CI 0.533–1.000), AUC value of 0.832 (95 % CI 0.642–0.979), and accuracy of 0.792 (95 % CI 0.625–0.958). Enrichment analysis of key genes indicated no significant enrichment in any known pathways.</p></div><div><h3>Conclusion</h3><p>Key genes with biological significance were identified based on the decrease in Gini coefficient within the Random Forest model. The combined use of Random Forest and Feedforward Neural Network to establish a diagnostic model showed good classification performance in Bipolar Disorder.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2024-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242124000691/pdfft?md5=bd0cf64abca37364e4ff55dbbc41772c&pid=1-s2.0-S2667242124000691-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141952844","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reduced ischemia‐reperfusion oxidative stress injury by melatonin and N‐acetylcysteine in the male rat brain","authors":"","doi":"10.1016/j.ibneur.2024.07.004","DOIUrl":"10.1016/j.ibneur.2024.07.004","url":null,"abstract":"<div><p>Middle cerebral artery occlusion (MCAO) is a model for inducing ischemic stroke in rodents, leading to devastating brain damage. Oxidative stress (OS) plays a crucial role in the pathogenesis of ischemia. In this study, the effect of melatonin and N-acetylcysteine on ischemia-reperfusion-induced oxidative stress injury in the cerebral cortex of male rats was investigated. 30 male Wistar rats were divided into sham, ischemic, NAC, melatonin and NAC + melatonin groups. All groups, except the sham group, underwent MCAO on the left side, and the treatment groups received intraperitoneal injections of either 50 mg/kg N-acetylcysteine (NAC) or 5 mg/kg melatonin or a combination of both 24 and 48 hours later. At 24 and 72 hours after surgery, the animals were examined for sensory and motor activity. The cerebral cortex was dissected after sacrificing the rats, infarct volume estimated and the concentrations of glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA) and nuclear factor erythroid-2 related factor 2 (Nrf2) were analyzed by enzyme-linked immunosorbent assay (ELISA). The results indicate that the NAC + melatonin group exhibited elevated sensory-motor activity and a reduced infarct volume rate in comparison to the ischemic group (p≤ 0.05). Compared to the ischemic group, the NAC + melatonin group showed a significant increase in SOD concentration and a significant decrease in MDA (p≤ 0.05). It can therefore be concluded that the simultaneous administration of NAC and melatonin can reduce the cerebral infarction volume, and improve neurological functions by modulating SOD and MDA.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2024-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242124000678/pdfft?md5=bd34eaf36ac6e60170151f6e01ae58d1&pid=1-s2.0-S2667242124000678-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141841929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}