Pub Date : 2024-11-19DOI: 10.1016/j.neulet.2024.138057
Daping Chen , Xin Zhou , Wanchao Yao , Fuwang Wang
Driving fatigue is a serious threat to driving safety. Therefore, it is of great significance to accurately detect driving fatigue. In this study, the generalized orthogonal partial directed coherence (gOPDC) algorithm, which measures the time–frequency domain interaction of electroencephalogram (EEG) signals, was used to accurately estimate the connectivity between cortical channels. The causal brain network of driver continuous driving is constructed. The results show that the clustering coefficient and global efficiency tend to decrease with the increase in driving time. Causal information flow in the left prefrontal, parietal, occipital regions and the right posterior frontal region increased significantly when subjects transitioned from awake to fatigued, while causal information flow in the right prefrontal, parietal, occipital regions and the left posterior frontal region decreased mutually significantly. Compared with the traditional driving fatigue algorithm, the accuracy of the method used in this paper is higher than the traditional methods.
{"title":"Causal brain network analysis of driving fatigue based on generalized orthogonalized partially directed coherence","authors":"Daping Chen , Xin Zhou , Wanchao Yao , Fuwang Wang","doi":"10.1016/j.neulet.2024.138057","DOIUrl":"10.1016/j.neulet.2024.138057","url":null,"abstract":"<div><div>Driving fatigue is a serious threat to driving safety. Therefore, it is of great significance to accurately detect driving fatigue. In this study, the generalized orthogonal partial directed coherence (gOPDC) algorithm, which measures the time–frequency domain interaction of electroencephalogram (EEG) signals, was used to accurately estimate the connectivity between cortical channels. The causal brain network of driver continuous driving is constructed. The results show that the clustering coefficient and global efficiency tend to decrease with the increase in driving time. Causal information flow in the left prefrontal, parietal, occipital regions and the right posterior frontal region increased significantly when subjects transitioned from awake to fatigued, while causal information flow in the right prefrontal, parietal, occipital regions and the left posterior frontal region decreased mutually significantly. Compared with the traditional driving fatigue algorithm, the accuracy of the method used in this paper is higher than the traditional methods.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"844 ","pages":"Article 138057"},"PeriodicalIF":2.5,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142682353","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}
Pub Date : 2024-11-17DOI: 10.1016/j.neulet.2024.138042
Elham Sanadgol , Morteza Zendehdel , Bita Vazir , Ali Rassouli , Hadi Haghbinnazarpak
Studies conducted on mammalian models have indicated the role of galanin-like peptide (GALP) in appetite regulation. For the first time, the present study examines the effects of this peptide on feed consumption and behavioral changes, as well as its interaction with dopaminergic and neuropeptide Y (NPY) systems in broilers. In experiment 1, broilers were injected with GALP (0.5, 1, and 2 μg) and saline. In experiment 2, saline, NPY1 receptor antagonist (BIBO-3304), GALP (2 μg), and BIBO-3304 + GALP were administrated. Experiments 3–6 were identical to experiment 2, except that NPY2 receptor antagonist (BIIE 0246), NPY5 receptor antagonist (CGP 71683A), D1 receptor antagonist (SCH39166), and D2 receptor antagonist (L-741,626) were injected instead of BIBO-3304. After that, cumulative meal consumption was recorded for 2 h. Also, behavioral changes in the broilers receiving GALP (0.5, 1, and 2 μg) were monitored for thirty minutes after infusion. Following the administration of GALP (1 and 2 μg), food intake and the number of feeding and exploratory pecks of chicks increased (P < 0.05), while other behaviors did not change significantly (P ≥ 0.05). Co-infusion of BIBO-3304 + GALP suppressed the orexigenic effect of GALP (P < 0.05). Infusion of BIIE 0246, CGP 71683A, and L-741,626 with GALP, had no significant effect on GALP-induced hyperphagia (P ≥ 0.05). However, the orexigenic effects of GALP were stimulated following the co-administration of SCH39166A + GALP (P < 0.05). These findings indicate that NPY1 and D1 receptors can mediate GALP-induced hyperphagia in broilers.
{"title":"Central administration of galanin-like peptide (GALP) causes short-term orexigenic effects in broilers: Mediatory role of NPY1 and D1 receptors","authors":"Elham Sanadgol , Morteza Zendehdel , Bita Vazir , Ali Rassouli , Hadi Haghbinnazarpak","doi":"10.1016/j.neulet.2024.138042","DOIUrl":"10.1016/j.neulet.2024.138042","url":null,"abstract":"<div><div>Studies conducted on mammalian models have indicated the role of galanin-like peptide (GALP) in appetite regulation. For the first time, the present study examines the effects of this peptide on feed consumption and behavioral changes, as well as its interaction with dopaminergic and neuropeptide Y (NPY) systems in broilers. In experiment 1, broilers were injected with GALP (0.5, 1, and 2 μg) and saline. In experiment 2, saline, NPY1 receptor antagonist (BIBO-3304), GALP (2 μg), and BIBO-3304 + GALP were administrated. Experiments 3–6 were identical to experiment 2, except that NPY2 receptor antagonist (BIIE 0246), NPY5 receptor antagonist (CGP 71683A), D1 receptor antagonist (SCH39166), and D2 receptor antagonist (L-741,626) were injected instead of BIBO-3304. After that, cumulative meal consumption was recorded for 2 h. Also, behavioral changes in the broilers receiving GALP (0.5, 1, and 2 μg) were monitored for thirty minutes after infusion. Following the administration of GALP (1 and 2 μg), food intake and the number of feeding and exploratory pecks of chicks increased (P < 0.05), while other behaviors did not change significantly (P ≥ 0.05). Co-infusion of BIBO-3304 + GALP suppressed the orexigenic effect of GALP (P < 0.05). Infusion of BIIE 0246, CGP 71683A, and L-741,626 with GALP, had no significant effect on GALP-induced hyperphagia (P ≥ 0.05). However, the orexigenic effects of GALP were stimulated following the co-administration of SCH39166A + GALP (P < 0.05). These findings indicate that NPY1 and D1 receptors can mediate GALP-induced hyperphagia in broilers.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"844 ","pages":"Article 138042"},"PeriodicalIF":2.5,"publicationDate":"2024-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142647837","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}
Pub Date : 2024-11-15DOI: 10.1016/j.neulet.2024.138039
Lauren I. Gulley Cox , Nicholas Dias , Chuan Zhang , Yingchun Zhang , Stacey L. Gorniak
With one in every four older adults living with T2D and one in every two older adults meeting the criteria for prediabetes, neuromuscular changes due to T2D are likely to impact functional activities in this population. Limited work in evaluating motor unit number and size across muscles in the upper extremity in persons with Type II Diabetes (T2D) exists, mostly due to the traditional belief bias that the upper extremity is relatively spared in T2D as compared to the lower extremities. The purpose of the current study was to evaluate motor unit number and size (using electrophysiological motor unit number index (MUNIX) and motor unit size index (MUSIX)) across the upper extremity in older adults with T2D (n = 13) as compared to healthy age- and sex-matched controls (n = 12). Persons with T2D presented with more motor units and larger motor unit sizes (p < 0.05) as compared to age- and sex-matched control participants. These changes were not dependent upon muscle location within a limb, indicating systemic neuromuscular changes associated with T2D. These group effects were clarified when health state covariates (e.g., blood pressure) were accounted for. Findings are consistent with emerging data that show altered neuromuscular characteristics with health state considerations in persons with T2D.
{"title":"Effects of Type II Diabetes on upper extremity muscle characteristics in older adults","authors":"Lauren I. Gulley Cox , Nicholas Dias , Chuan Zhang , Yingchun Zhang , Stacey L. Gorniak","doi":"10.1016/j.neulet.2024.138039","DOIUrl":"10.1016/j.neulet.2024.138039","url":null,"abstract":"<div><div>With one in every four older adults living with T2D and one in every two older adults meeting the criteria for prediabetes, neuromuscular changes due to T2D are likely to impact functional activities in this population. Limited work in evaluating motor unit number and size across muscles in the upper extremity in persons with Type II Diabetes (T2D) exists, mostly due to the traditional belief bias that the upper extremity is relatively spared in T2D as compared to the lower extremities. The purpose of the current study was to evaluate motor unit number and size (using electrophysiological motor unit number index (MUNIX) and motor unit size index (MUSIX)) across the upper extremity in older adults with T2D (n = 13) as compared to healthy age- and sex-matched controls (n = 12). Persons with T2D presented with more motor units and larger motor unit sizes (p < 0.05) as compared to age- and sex-matched control participants. These changes were not dependent upon muscle location within a limb, indicating systemic neuromuscular changes associated with T2D. These group effects were clarified when health state covariates (e.g., blood pressure) were accounted for. Findings are consistent with emerging data that show altered neuromuscular characteristics with health state considerations in persons with T2D.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"844 ","pages":"Article 138039"},"PeriodicalIF":2.5,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142644605","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}
Nociception is defined as “the neural process of encoding noxious stimuli” by the International Association for the Study of Pain (IASP). Nociception relies on detecting noxious stimuli arising from a potentially or actually tissue-damaging event via specialized cells called nociceptors. In planarians, nociceptive behavior is often indicated by a ‘scrunching’ gait, in contrast to the usual gliding behavior displayed in normal conditions. The present study extends our previous study Reho et al. (2024) by testing a new potentially irritant molecule, Cinnamaldehyde (CA), which could induce scrunching gaits. We reproduced the nociceptive chemical tests from our previous study using CA instead of Allyl isothiocyanate (AITC) on Girardia dorotocephala (Gd) implementing an open field behavioral analysis. CA induced a dose-dependent increase in scrunching gait similar to the action of AITC and was expectedly partially suppressed by morphine and meloxicam. Knocking down the expression of the Gd-TRPA1 ion channel by RNA interference also suppressed the behavioral reaction to the molecule. In conclusion, we demonstrated that CA induced a nociceptive behavior in planarians through an action on the ion channel TRPA1.
{"title":"Cinnamaldehyde induces a TRPA1-mediated nociceptive behavior in planarians","authors":"Rémy Morana, Bénédicte Darbon, Lalee Herrmann, Yannick Menger, Guillaume Reho, Hervé Cadiou","doi":"10.1016/j.neulet.2024.138041","DOIUrl":"10.1016/j.neulet.2024.138041","url":null,"abstract":"<div><div>Nociception is defined as “the neural process of encoding noxious stimuli” by the International Association for the Study of Pain (IASP). Nociception relies on detecting noxious stimuli arising from a potentially or actually tissue-damaging event via specialized cells called nociceptors. In planarians, nociceptive behavior is often indicated by a ‘scrunching’ gait, in contrast to the usual gliding behavior displayed in normal conditions. The present study extends our previous study Reho et al. (2024) by testing a new potentially irritant molecule, Cinnamaldehyde (CA), which could induce scrunching gaits. We reproduced the nociceptive chemical tests from our previous study using CA instead of Allyl isothiocyanate (AITC) on <em>Girardia dorotocephala</em> (<em>Gd</em>) implementing an open field behavioral analysis. CA induced a dose-dependent increase in scrunching gait similar to the action of AITC and was expectedly partially suppressed by morphine and meloxicam. Knocking down the expression of the Gd-TRPA1 ion channel by RNA interference also suppressed the behavioral reaction to the molecule. In conclusion, we demonstrated that CA induced a nociceptive behavior in planarians through an action on the ion channel TRPA1.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"844 ","pages":"Article 138041"},"PeriodicalIF":2.5,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142644604","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}
Pub Date : 2024-11-13DOI: 10.1016/j.neulet.2024.138040
Huy Lu , Nicole Roeder , Brittany Richardson , John Hamilton , Abhisheak Sharma , Yuji Owada , Yoshiteru Kagawa , Panayotis Thanos
Fatty acid-binding protein 7 (FABP7) aids in the intracellular transport of endogenous cannabinoids and is involved in regulating the stress response system. This study examined the role of FABP7 in chronic stress exposure through the binding of CB1 receptors. Adult male FABP7+/+ and FABP7-/- mice were treated with the unpredictable chronic mild stress (UCMS) procedure. After 28 days of treatment, mice were euthanized, and CB1 was measured with in vitro autoradiography using [3H] SR141716A. FABP7-/- mice, irrespective of stress treatment, showed reduced [3H] SR141716A binding in the amygdala, secondary somatosensory cortex, and ventral caudate putamen compared with the FABP7+/+ mice. Additionally, FABP7-/- mice treated with UCMS exhibited a reduction in CB1 binding in the globus pallidus and ventral caudate putamen compared with UCMS-treated FABP7+/+ mice. Genetic deletion of FABP7 can decrease CB1 expression in various brain regions; however, the underlying mechanism remains unclear.
{"title":"Fatty acid-binding protein 7 gene deletion promotes decreases in brain cannabinoid type 1 receptor binding","authors":"Huy Lu , Nicole Roeder , Brittany Richardson , John Hamilton , Abhisheak Sharma , Yuji Owada , Yoshiteru Kagawa , Panayotis Thanos","doi":"10.1016/j.neulet.2024.138040","DOIUrl":"10.1016/j.neulet.2024.138040","url":null,"abstract":"<div><div>Fatty acid-binding protein 7 (FABP7) aids in the intracellular transport of endogenous cannabinoids and is involved in regulating the stress response system. This study examined the role of FABP7 in chronic stress exposure through the binding of CB1 receptors. Adult male FABP7<sup>+/+</sup> and FABP7<sup>-/-</sup> mice were treated with the unpredictable chronic mild stress (UCMS) procedure. After 28 days of treatment, mice were euthanized, and CB1 was measured with in vitro autoradiography using [3H] SR141716A. FABP7<sup>-/-</sup> mice, irrespective of stress treatment, showed reduced [3H] SR141716A binding in the amygdala, secondary somatosensory cortex, and ventral caudate putamen compared with the FABP7<sup>+/+</sup> mice. Additionally, FABP7<sup>-/-</sup> mice treated with UCMS exhibited a reduction in CB1 binding in the globus pallidus and ventral caudate putamen compared with UCMS-treated FABP7<sup>+/+</sup> mice. Genetic deletion of FABP7 can decrease CB1 expression in various brain regions; however, the underlying mechanism remains unclear.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"844 ","pages":"Article 138040"},"PeriodicalIF":2.5,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624611","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}
Pub Date : 2024-11-12DOI: 10.1016/j.neulet.2024.138038
Feyza Alyu Altinok , Ilhem Dallali , Abderaouf Boubekka , Ahmed Hasan , Yusuf Ozturk
DRG primary neuron cultures, derived from rodents, closely mimic properties of sensory neurons in vivo and are highly useful for studying pain and neurological disorders. These cultures are pivotal in patch-clamp electrophysiology for sensory neuron properties analysis. A detailed, replicable protocol in scientific research ensures experiment accuracy and reproducibility. This paper provides comprehensive details for replicating the protocol and achieving consistent results in primary DRG cell culture as used for patch-clamp recordings. We outlined a comprehensive protocol for establishing primary DRG cell culture, optimized for improved gigaseal formation in whole-cell patch-clamp recordings. Additionally, we conducted a simulation study focused on recording macroscopic K+ channels. The findings established an optimized novel protocol that works reliably for whole-cell patch-clamp recordings and data analysis using primary DRG cells prepared as described in this publication. The details for the protocol in the literature are dispersed across various publications, making it challenging to find a comprehensive summary in one source. This study confirms, for the first time, the efficacy of using fewer protocol steps, which reduces stress and variability in obtaining suitable cells for patch-clamp recordings compared to existing methods in the literature. Given the challenges posed by the dissociation process of primary DRG cells and the importance of comprehensive method documentation in the literature, the protocol presented provides improved and consistent applications of primary DRG cell culture in patch-clamp recordings.
{"title":"Optimized primary dorsal root ganglion cell culture protocol for reliable K+ current patch-clamp recordings","authors":"Feyza Alyu Altinok , Ilhem Dallali , Abderaouf Boubekka , Ahmed Hasan , Yusuf Ozturk","doi":"10.1016/j.neulet.2024.138038","DOIUrl":"10.1016/j.neulet.2024.138038","url":null,"abstract":"<div><div>DRG primary neuron cultures, derived from rodents, closely mimic properties of sensory neurons <em>in vivo</em> and are highly useful for studying pain and neurological disorders. These cultures are pivotal in patch-clamp electrophysiology for sensory neuron properties analysis. A detailed, replicable protocol in scientific research ensures experiment accuracy and reproducibility. This paper provides comprehensive details for replicating the protocol and achieving consistent results in primary DRG cell culture as used for patch-clamp recordings. We outlined a comprehensive protocol for establishing primary DRG cell culture, optimized for improved gigaseal formation in whole-cell patch-clamp recordings. Additionally, we conducted a simulation study focused on recording macroscopic K<sup>+</sup> channels. The findings established an optimized novel protocol that works reliably for whole-cell patch-clamp recordings and data analysis using primary DRG cells prepared as described in this publication. The details for the protocol in the literature are dispersed across various publications, making it challenging to find a comprehensive summary in one source. This study confirms, for the first time, the efficacy of using fewer protocol steps, which reduces stress and variability in obtaining suitable cells for patch-clamp recordings compared to existing methods in the literature. Given the challenges posed by the dissociation process of primary DRG cells and the importance of comprehensive method documentation in the literature, the protocol presented provides improved and consistent applications of primary DRG cell culture in patch-clamp recordings.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"844 ","pages":"Article 138038"},"PeriodicalIF":2.5,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624623","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}
Mesenchymal stem cell (MSC)-based therapy has been applied in several clinical trials of spinal cord injury (SCI). We have successfully established MSCs from human cranial bone and developed a longitudinal neuromonitoring technique for rodents. In addition to single transplantation, the potential of multiple transplantations has been suggested as a new therapeutic strategy. However, there are no reports on the electrophysiological effects of multiple MSC transplantations in SCI using transcranial electrical stimulation motor-evoked potentials (tcMEPs). Here, we aimed to elucidate the efficacy and mechanism of action of multiple MSC transplantations using tcMEPs. After establishing a weight-drop-induced SCI rat model, we performed repeated intravenous transplantation of human cranial bone-derived MSCs (hcMSCs) on days 1 and 3 post-SCI. Motor function and tcMEP recovery were evaluated 6 weeks post-transplantation. Tissue repair post-SCI was assessed using immunostaining for myelin and neurons in the injured posterior cord. Repeated hcMSC transplantation significantly improved motor function and electrophysiological recovery compared to single transplantation and control treatment. Repeated hcMSC transplantation promoted electrophysiological functional recovery by exerting a protective effect on the functional structure of pyramidal tract axons. Thus, acute-phase repeated transplantation could be a novel and effective therapeutic strategy for the clinical application of MSCs in SCI.
{"title":"Repeated human cranial bone-derived mesenchymal stem cell transplantation improved electrophysiological recovery in a spinal cord injury rat model","authors":"Yuyo Maeda , Takafumi Mitsuhara , Masaaki Takeda , Misaki Okamoto , Takashi Otsuka , Takeshi Hara , Masashi Kuwabara , Nobutaka Horie","doi":"10.1016/j.neulet.2024.138031","DOIUrl":"10.1016/j.neulet.2024.138031","url":null,"abstract":"<div><div>Mesenchymal stem cell (MSC)-based therapy has been applied in several clinical trials of spinal cord injury (SCI). We have successfully established MSCs from human cranial bone and developed a longitudinal neuromonitoring technique for rodents. In addition to single transplantation, the potential of multiple transplantations has been suggested as a new therapeutic strategy. However, there are no reports on the electrophysiological effects of multiple MSC transplantations in SCI using transcranial electrical stimulation motor-evoked potentials (tcMEPs). Here, we aimed to elucidate the efficacy and mechanism of action of multiple MSC transplantations using tcMEPs. After establishing a weight-drop-induced SCI rat model, we performed repeated intravenous transplantation of human cranial bone-derived MSCs (hcMSCs) on days 1 and 3 post-SCI. Motor function and tcMEP recovery were evaluated 6 weeks post-transplantation. Tissue repair post-SCI was assessed using immunostaining for myelin and neurons in the injured posterior cord. Repeated hcMSC transplantation significantly improved motor function and electrophysiological recovery compared to single transplantation and control treatment. Repeated hcMSC transplantation promoted electrophysiological functional recovery by exerting a protective effect on the functional structure of pyramidal tract axons. Thus, acute-phase repeated transplantation could be a novel and effective therapeutic strategy for the clinical application of MSCs in SCI.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"844 ","pages":"Article 138031"},"PeriodicalIF":2.5,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624630","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}
Pub Date : 2024-11-06DOI: 10.1016/j.neulet.2024.138037
Yue-Wei Xu , Chang-Heng Yao , Xiao-Ming Gao , Li Wang , Meng-Xiang Zhang , Xiao-Dan Yang , Jing Li , Wen-Ling Dai , Man-Qin Yang , Ming Cai
Background
Cerebral ischemia/reperfusion (I/R) injury is a serious vascular disease with extremely high mortality and disability rate. Bakuchiol (BAK) was found in leaves and seeds of Psoralea corylifolia Linn and has been shown to decrease inflammation and reduce oxidative stress, while the mechanism of BAK in ameliorating cerebral I/R injury remains unclear.
Methods
Middle cerebral artery occlusion reperfusion (MACO/R) was used to establish mouse model. The protective effect of BAK in MCAO/R mices was detected by performing neurological deficit testing, TTC staining, and H&E staining. Oxygen/glucose deprivation and reperfusion (OGD/R) was used to stimulate SH-SY5Y cells in vitro. Protein expression was detected by western blotting, gene expression was detected by quantitative real-time polymerase chain reaction and apoptosis was detected by immunofluorescence.
Results
Our study indicated that BAK protected ischemia–reperfusion injury in MACO/R mice, and upregulated superoxide dismutase (SOD) and the catalase (CAT) enzyme activity. BAK also inhibited the expression of TNF-α, IL-1β, IL-6, and IL-18 and suppressed apoptosis and pyroptosis both in MACO/R mice and in OGD/R SH-SY5Y cells. Further results showed that BAK could suppress TXNIP, ASC, NLRP3, and caspase-1 mRNA levels to reverse assembly of inflammasome. And BAK could also upregulate the expression of phosphorylated AMP-activated protein kinase (AMPK) and nuclear factor erythroid 2-related factor (Nrf2). In addition, Nrf2 inhibitor ML385 reversed the BAK induced reduction of TXNIP, ASC, NLRP3, and the AMPK inhibitor also abolished BAK’ the effect on the regulation of Nrf2, TXNIP, ASC, NLRP3, caspase-1, and pro-inflammatory cytokines. In conclusion, BAK, found in leaves and seeds of Psoralea corylifolia Linn, could ameliorated cerebral I/R injury through activating AMPK/Nrf2 to inhibit NLRP3 inflammasome, which might present new therapeutic strategy for cerebral I/R injury.
{"title":"BAK ameliorated cerebral infarction/ischemia–reperfusion injury by activating AMPK/Nrf2 to inhibit TXNIP/NLRP3/caspase-1 axis","authors":"Yue-Wei Xu , Chang-Heng Yao , Xiao-Ming Gao , Li Wang , Meng-Xiang Zhang , Xiao-Dan Yang , Jing Li , Wen-Ling Dai , Man-Qin Yang , Ming Cai","doi":"10.1016/j.neulet.2024.138037","DOIUrl":"10.1016/j.neulet.2024.138037","url":null,"abstract":"<div><h3>Background</h3><div>Cerebral ischemia/reperfusion (I/R) injury is a serious vascular disease with extremely high mortality and disability rate. Bakuchiol (BAK) was found in leaves and seeds of <em>Psoralea corylifolia</em> Linn and has been shown to decrease inflammation and reduce oxidative stress, while the mechanism of BAK in ameliorating cerebral I/R injury remains unclear.</div></div><div><h3>Methods</h3><div>Middle cerebral artery occlusion reperfusion (MACO/R) was used to establish mouse model. The protective effect of BAK in MCAO/R mices was detected by performing neurological deficit testing, TTC staining, and H&E staining. Oxygen/glucose deprivation and reperfusion (OGD/R) was used to stimulate SH-SY5Y cells <em>in vitro</em>. Protein expression was detected by western blotting, gene expression was detected by quantitative real-time polymerase chain reaction and apoptosis was detected by immunofluorescence.</div></div><div><h3>Results</h3><div>Our study indicated that BAK protected ischemia–reperfusion injury in MACO/R mice, and upregulated superoxide dismutase (SOD) and the catalase (CAT) enzyme activity. BAK also inhibited the expression of TNF-α, IL-1β, IL-6, and IL-18 and suppressed apoptosis and pyroptosis both in MACO/R mice and in OGD/R SH-SY5Y cells. Further results showed that BAK could suppress TXNIP, ASC, NLRP3, and caspase-1 mRNA levels to reverse assembly of inflammasome. And BAK could also upregulate the expression of phosphorylated AMP-activated protein kinase (AMPK) and nuclear factor erythroid 2-related factor (Nrf2). In addition, Nrf2 inhibitor ML385 reversed the BAK induced reduction of TXNIP, ASC, NLRP3, and the AMPK inhibitor also abolished BAK’ the effect on the regulation of Nrf2, TXNIP, ASC, NLRP3, caspase-1, and pro-inflammatory cytokines. In conclusion, BAK, found in leaves and seeds of <em>Psoralea corylifolia</em> Linn, could ameliorated cerebral I/R injury through activating AMPK/Nrf2 to inhibit NLRP3 inflammasome, which might present new therapeutic strategy for cerebral I/R injury.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"844 ","pages":"Article 138037"},"PeriodicalIF":2.5,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624616","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}
Pub Date : 2024-11-05DOI: 10.1016/j.neulet.2024.138036
Shiva Alipour , Ali Aghebati-Maleki , Mohammad Reza Sadeghi , Mohammad Sadegh Soltani-Zangbar , Ali Khakpour , Leili Aghebati-Maleki
A critical component in triggering and progressing autoimmune multiple sclerosis (MS) is the deregulation of immune responses, including dysfunction of T regulatory cells (Tregs), critical participants in the pathogenetic context of inflammation. It has been found that miRNAs have a crucial role in the induction of MS because dysregulation of miRNAs can result in defects in immunological tolerance. In this investigation, we examined the miR-10a contribution to MS disorder by comparing the altered expression of miR-10a in peripheral blood mononuclear cells (PBMCs) of 40 MS patients to 40 healthy controls. Additionally, we examined Tregs’ frequency in MS patients in compare with healthy controls. We evaluated the secreted levels of anti-inflammatory cytokines, such as IL-10 and TGF-B, in the serum of MS patients and their expression level in healthy controls’ and patients’ peripheral blood mononuclear cells (PBMCs). Then, we assessed the correlation between miR-10a expression with Treg frequency and levels of anti-inflammatory cytokines in serum. PBMCs from MS patients had downregulated expression of miR-10a, and a substantial correlation was found between this expression and a reduction in Treg cells’ frequency and the secreted anti-inflammatory cytokines associated with Tregs’ diminished functionality. In summary, our research demonstrated a strong correlation between Tregs’ frequency, lower levels of cytokines linked to Treg function, and lower expression of miR-10a in PBMCs. So, the alteration of miR-10a can be utilized as a probable therapeutic target for the prevention and management of MS disorder. However, further examination is requisite before this strategy become practical for use in the clinical setting.
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Pub Date : 2024-11-04DOI: 10.1016/j.neulet.2024.138035
Yicheng Wang , Yongli Wang , Guangxin Yue , Jingjing Lin , Xueying Liu , Liwei Wang , Yonglie Zhao
Objective
To evaluate the effects of Ligustrazine (Lig) on nitroglycerin-induced migraine and explore the mechanism through the mitochondria-inflammation pathway.
Methods
Rats were divided into control, model, Lig(50 mg/kg) + Erastin, Lig(100 mg/kg), Lig(50 mg/kg), and Zolmitriptan groups. Nitroglycerin (NTG) was administered through injection to trigger a migraine. The following parameters were measured: mechanical pain threshold, mitochondrial morphology, levels of reactive oxygen species (ROS), mitochondrial membrane potential (MMP), Adenosine triphosphate (ATP), and Nitric oxide (NO). The neuronal nitric oxide synthase (nNOS), transient receptor potential A1 (TRPA1), interleukin 1 beta (IL-1β), nuclear factor-kappaB (NF-κB), and calcitonin gene-related peptide (CGRP) were detected by Western blotting and immunohistochemistry.
Results
Compared with the model group, the Lig(100 mg/kg) and Lig(50 mg/kg) groups increased mechanical pain threshold as well as improved abnormal mitochondrial morphology. Moreover, compared with the model group, the Lig(100 mg/kg) and Lig(50 mg/kg) groups demonstrated reduced levels of ROS, and NO, and increased MMP, and ATP. Lig(100 mg/kg) and Lig(50 mg/kg) groups reduced inflammation and oxidative stress by inhibiting certain gene expressions. When Erastin was injected, the effectiveness of Lig decreased, indicating that Lig’s therapeutic effect was related to the extent of mPTP opening.
Conclusion
The mitochondria-inflammation pathway plays a critical role in regulating migraine. Lig exerts anti-migraine effects primarily by modulating the mitochondria-inflammation pathway providing a novel perspective on migraine research that is beneficial for its clinical application.
目的评估利格列净（Lig）对硝酸甘油诱导的偏头痛的影响，并探讨其通过线粒体-炎症途径的机制：大鼠分为对照组、模型组、Lig（50 mg/kg）+Erastin组、Lig（100 mg/kg）组、Lig（50 mg/kg）组和Zolmitriptan组。通过注射硝酸甘油（NTG）引发偏头痛。对以下参数进行了测量：机械痛阈值、线粒体形态、活性氧（ROS）水平、线粒体膜电位（MMP）、三磷酸腺苷（ATP）和一氧化氮（NO）。通过 Western 印迹和免疫组织化学方法检测了神经元一氧化氮合酶（nNOS）、瞬时受体电位 A1（TRPA1）、白细胞介素 1 beta（IL-1β）、核因子-卡巴（NF-κB）和降钙素基因相关肽（CGRP）：结果：与模型组相比，Lig（100 mg/kg）组和Lig（50 mg/kg）组提高了机械痛阈，改善了线粒体的异常形态。此外，与模型组相比，Lig（100 毫克/千克）组和 Lig（50 毫克/千克）组的 ROS 和 NO 水平降低，MMP 和 ATP 水平升高。Lig（100 毫克/千克）组和 Lig（50 毫克/千克）组通过抑制某些基因的表达减少了炎症和氧化应激。当注射 Erastin 时，Lig 的效果下降，这表明 Lig 的治疗效果与 mPTP 的开放程度有关：结论：线粒体-炎症通路在调节偏头痛中起着关键作用。Lig主要通过调节线粒体-炎症途径发挥抗偏头痛作用，为偏头痛研究提供了一个新的视角，有利于偏头痛的临床应用。
{"title":"Effects of ligustrazine on energy metabolism in migraine rats based on mitochondria-inflammation pathway","authors":"Yicheng Wang , Yongli Wang , Guangxin Yue , Jingjing Lin , Xueying Liu , Liwei Wang , Yonglie Zhao","doi":"10.1016/j.neulet.2024.138035","DOIUrl":"10.1016/j.neulet.2024.138035","url":null,"abstract":"<div><h3>Objective</h3><div>To evaluate the effects of Ligustrazine (Lig) on nitroglycerin-induced migraine and explore the mechanism through the mitochondria-inflammation pathway.</div></div><div><h3>Methods</h3><div>Rats were divided into control, model, Lig(50 mg/kg) + Erastin, Lig(100 mg/kg), Lig(50 mg/kg), and Zolmitriptan groups. Nitroglycerin (NTG) was administered through injection to trigger a migraine. The following parameters were measured: mechanical pain threshold, mitochondrial morphology, levels of reactive oxygen species (ROS), mitochondrial membrane potential (MMP), Adenosine triphosphate (ATP), and Nitric oxide (NO). The neuronal nitric oxide synthase (nNOS), transient receptor potential A1 (TRPA1), interleukin 1 beta (IL-1β), nuclear factor-kappaB (NF-κB), and calcitonin gene-related peptide (CGRP) were detected by Western blotting and immunohistochemistry.</div></div><div><h3>Results</h3><div>Compared with the model group, the Lig(100 mg/kg) and Lig(50 mg/kg) groups increased mechanical pain threshold as well as improved abnormal mitochondrial morphology. Moreover, compared with the model group, the Lig(100 mg/kg) and Lig(50 mg/kg) groups demonstrated reduced levels of ROS, and NO, and increased MMP, and ATP. Lig(100 mg/kg) and Lig(50 mg/kg) groups reduced inflammation and oxidative stress by inhibiting certain gene expressions. When Erastin was injected, the effectiveness of Lig decreased, indicating that Lig’s therapeutic effect was related to the extent of mPTP opening.</div></div><div><h3>Conclusion</h3><div>The mitochondria-inflammation pathway plays a critical role in regulating migraine. Lig exerts anti-migraine effects primarily by modulating the mitochondria-inflammation pathway providing a novel perspective on migraine research that is beneficial for its clinical application.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"844 ","pages":"Article 138035"},"PeriodicalIF":2.5,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142591283","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}
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