Journal of chemical neuroanatomy最新文献

{"title":"Neurobiological and pathophysiological concepts of Christfried Jakob (1866–1956) on language and aphasia: An English translation of two communications [1910,1932] and a modern perspective","authors":"Maria E. Vasilopoulou ,&nbsp;Lazaros C. Triarhou","doi":"10.1016/j.jchemneu.2023.102341","DOIUrl":"10.1016/j.jchemneu.2023.102341","url":null,"abstract":"<div><p><span>The aim of the present article is to preserve, in English translation, two historical communications on aphasia and the pathophysiology of language by the neurobiologist Christfried Jakob (1866–1956) of Buenos Aires, and to place them in a modern perspective. The morphofunctional basis of human language and its pathology occupied Jakob’s mind over three decades. His synthetic conclusions were based on the neuropathological examination of dozens of aphasic cases from the Hospital de Las Mercedes and the National Women’s Psychiatric Hospital between 1906 and 1936. Special mention is made of the role of the </span>cerebellum<span><span>, the thalamus, and their connections with the </span>cerebral cortex, and the language network. Current research and imaging studies support and elaborate that which Jacob presented so many years ago; many of his analyses and ideas are informative and remain relevant today.</span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"133 ","pages":"Article 102341"},"PeriodicalIF":2.8,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10286434","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}

{"title":"Involvement of iNOS-induced reactive enteric glia cells in gastrointestinal motility disorders of postoperative Ileus mice","authors":"Ailing Sun ,&nbsp;An Hu ,&nbsp;Jialing Lin ,&nbsp;Linan Wang ,&nbsp;Chuangbo Xie ,&nbsp;Yongyong Shi ,&nbsp;Qingxiong Hong ,&nbsp;Gaofeng Zhao","doi":"10.1016/j.jchemneu.2023.102312","DOIUrl":"10.1016/j.jchemneu.2023.102312","url":null,"abstract":"<div><p><span>Postoperative ileus (POI) is the cessation or reduction of gastrointestinal (GI) motility after surgery. Reactive enteric glial cells<span><span> (EGCs) are critical for maintaining bowel function. However, the triggering mechanisms and downstream effects of reactive EGCs in POI were poorly understood. The goal of this current study was to investigate whether the </span>inducible nitric oxide synthase (iNOS)-driven reactive EGCs participated in GI motility disorders and mechanisms underlying altered GI motility in POI. Intestinal manipulation (IM)-induced POI mice and iNOS</span></span>^−/−<span> mice were used in the study. Longitudinal muscle and myenteric plexuses (LMMPs) from the distal small intestine<span> were stained by immunofluorescence. Our results found that the GI motility disorders occurred in the IM-induced POI mice, and reactive EGCs were observed in LMMPs. Glial metabolic inhibitor gliotoxin<span><span> fluorocitrate (FC) treatment or iNOS gene knockout attenuated GI motility dysfunction. In addition, we also found that FC treatment or iNOS gene knockout significantly inhibited the fluorescence intensity macrophage colony-stimulating factor (M-CSF), which reduced M2 phenotype </span>macrophages activation<span> in LMMPs of IM-induced POI mice. Our findings demonstrated that iNOS-driven reactive EGCs played a key role and were tightly linked to the MMs homeostasis in the POI mice. EGCs are emerging as a new frontier in neurogastroenterology and a potential therapeutic target.</span></span></span></span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"133 ","pages":"Article 102312"},"PeriodicalIF":2.8,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10144097","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}

{"title":"Thimet oligopeptidase (THOP 1) distribution in cane toad (Bufo Marinus, Linnaeus, 1758) brain","authors":"Diogo M.L.P. Cavalcanti ,&nbsp;Tiago S. Teófilo ,&nbsp;Tayline D. Rodrigues ,&nbsp;Tayssa N.S. Barbosa ,&nbsp;José D. Fontenele-Neto","doi":"10.1016/j.jchemneu.2023.102345","DOIUrl":"10.1016/j.jchemneu.2023.102345","url":null,"abstract":"<div><p><span><span>Thimet oligopeptides (THOP 1) is a metal-dependent </span>peptidase<span><span> involved in the metabolism of neuropeptides and the presentation of peptides via MHC-1. It has been shown to play a role in the regulation of protein-protein interactions and the metabolism of intracellular peptides. THOP 1 is associated with important </span>biological processes<span> such as metabolism and neurodegenerative diseases, among others. The objective of this study is to elucidate the distribution of THOP 1 in the </span></span></span><span><em>Bufo marinus</em></span><span> brain. The analysis of THOP 1 amino acid sequences<span> indicates that they have been conserved throughout evolution, with significant homology observed across various phyla. When comparing amphibians with other species, more than 70% identity can be identified. Immunohistochemistry<span> analysis of the toad's brain has demonstrated that the enzyme has a ubiquitous distribution, consistent with previous findings in mammals. THOP 1 can be found in important areas of the brain, such as bulb, thalamic nuclei, striatum, hypothalamus, and among others. Nonetheless, THOP 1 is consistently localized within the nucleus, a pattern also observed in the rat brain. Therefore, based on these results, the toad appears to be an excellent model for studying the general biology of THOP 1, given the substantial homology of this enzyme with mammals and its similarity in distribution within the brain.</span></span></span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"133 ","pages":"Article 102345"},"PeriodicalIF":2.8,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41130712","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}

{"title":"Exploring the effects of embryonic and neonatal exposure to lipopolysaccharides on oligodendrocyte differentiation in the rat hippocampus and the protective effect of alpha-glycosyl isoquercitrin","authors":"Hiromu Okano ,&nbsp;Ryota Ojiro ,&nbsp;Xinyu Zou ,&nbsp;Qian Tang ,&nbsp;Shunsuke Ozawa ,&nbsp;Mihoko Koyanagi ,&nbsp;Robert R. Maronpot ,&nbsp;Toshinori Yoshida ,&nbsp;Makoto Shibutani","doi":"10.1016/j.jchemneu.2023.102336","DOIUrl":"10.1016/j.jchemneu.2023.102336","url":null,"abstract":"<div><p><span>This study compared the effects of embryonic and neonatal lipopolysaccharides<span><span> (LPS) exposure (E-LPS and N-LPS) on oligodendrocyte<span> (OL) differentiation in the hippocampus of male rats and explored the protective effect of the antioxidant alpha-glycosyl </span></span>isoquercitrin<span> (AGIQ). Using SD rats, LPS exposure occurred either intraperitoneally in dams between gestational days 15 and 16 (50 µg/kg body weight/time) or in male pups on postnatal day (PND) 3 (1 mg/kg body weight). Under both regimens, AGIQ at 0.5% (w/w) was supplemented, to dams from the gestation period (before LPS exposure) until weaning on PND 21 and to male offspring from weaning until PND 77 (adulthood). Compared with a control treatment, E-LPS treatment resulted in fewer NG2</span></span></span>⁺<span> OL progenitor cells (OPCs) and an upregulation of </span><em>Tcf4</em> at PND 6; by PND 21, low NG2⁺ OPC number persisted, but OLIG2⁺<span> OL lineage cells increased, while CNPase</span>⁺ mature OLs counts were unchanged. By contrast, N-LPS treatment resulted in fewer OLIG2⁺ cells and an upregulation of <em>Bmp4</em> at PND 6; by PND 21, NG2⁺ OPCs decreased, while GFAP⁺ astrocytes increased at both PND 6 and 21. After N-LPS treatment, <em>Kl</em> and <em>Yy1</em> were downregulated and there were fewer Klotho⁺ and CNPase⁺<span> cells at PND 21. Results suggest that E-LPS treatment facilitates OPC differentiation into pre- and immature OLs until weaning, while N-LPS treatment suppresses OPC differentiation into mature OLs but facilitates astrocyte generation; however, these changes spontaneously recovered by adulthood under both regimens. AGIQ treatment ameliorated the effects of LPS treatment of both regimens, suggesting that LPS-induced disruption of OPC/OL differentiation occurs via neuroinflammation.</span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"133 ","pages":"Article 102336"},"PeriodicalIF":2.8,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10284104","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}

{"title":"Activation patterns of dopaminergic cell populations reflect different learning scenarios in a cichlid fish, Pseudotropheus zebra","authors":"Calvo Roberta ,&nbsp;Schluessel Vera ,&nbsp;Hofmann Hans A ,&nbsp;Hofmann Michael H","doi":"10.1016/j.jchemneu.2023.102342","DOIUrl":"10.1016/j.jchemneu.2023.102342","url":null,"abstract":"<div><p><span>Dopamine is present in all vertebrates and the functional roles of the subsystems are assumed to be similar. Whereas the effect of dopaminergic modulation is well investigated in different target systems, less is known about the factors that are causing the modulation of dopaminergic cells. Using the zebra mbuna, </span><em>Pseudotropheus zebra</em><span>, a cichlid fish<span><span><span> from Lake Malawi as a model system, we investigated the activation of specific dopaminergic cell populations detected by double-labeling with TH and pS6 antibodies while the animals were solving different learning tasks. Specifically, we compared an intense </span>avoidance learning situation, an instrumental learning task, and a non-learning isolated group and found strong activation of different dopaminergic cell populations. Preoptic-hypothalamic cell populations respond to the stress component in the avoidance task, and the forced movement/locomotion may be responsible for activation in the posterior tubercle. The instrumental learning task had little stress component, but the activation of the raphe superior in this group may be correlated with attention or arousal during the training sessions. At the same time, the weaker activation of the nucleus of the </span>posterior commissure may be related to positive reward acting onto tectal circuits. Finally, we examined the co-activation patterns across all dopaminergic cell populations and recovered robust differences across experimental groups, largely driven by hypothalamic, posterior tubercle, and brain stem regions possibly encoding the valence and salience associated with stressful stimuli. Taken together, our results offer some insights into the different functions of the dopaminergic cell populations in the brain of a non-mammalian vertebrate in correlation with different behavioral conditions, extending our knowledge for a more comprehensive view of the mechanisms of dopaminergic modulation in vertebrates.</span></span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"133 ","pages":"Article 102342"},"PeriodicalIF":2.8,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10300995","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}

{"title":"The potential effect of salvianolic acid B against rat ischemic brain injury in combination with mesenchymal stem cells","authors":"Minli Yan ,&nbsp;Zheming Li ,&nbsp;Shijie Dai ,&nbsp;Shouye Li ,&nbsp;Pingping Yu","doi":"10.1016/j.jchemneu.2023.102338","DOIUrl":"10.1016/j.jchemneu.2023.102338","url":null,"abstract":"<div><h3>Background</h3><p>Mesenchymal stem cells (MSCs) and Salvianolic acid B (SAB) are known to exert potent anti-inflammatory and anti-oxidative properties. But the effect of SAB and MSCs combination treatment on the cerebral ischemia/reperfusion injury (CI/RI) is not clear.</p></div><div><h3>Methods</h3><p>After the CI/RI animal model<span> established, rats were administered with MSCs and SAB individually or combination treatment. To evaluate the therapeutic potential, behavioral tests, TTC staining<span>, Hematoxylin-eosin (HE) staining, and immunofluorescence assays were performed to evaluate the neuroprotection<span><span><span><span> and endogenous neurogenesis. </span>Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining and </span>enzyme linked immunosorbent assay (ELISA) were performed to evaluate the anti-apoptosis and anti-inflammatory effect. Meanwhile, the expression of the TLR4/NF-ĸB/MYD88 signal pathway-related proteins was evaluated by </span>Western blot.</span></span></span></p></div><div><h3>Results</h3><p><span>MSCs and SAB individually or combination treatment have protective effect in CI/RI rats. More importantly, the rats with the combination treatment showed a better behavioral recovery, neurogenesis and smaller infarct size compared with the rats administered with MSCs or SAB individually. Further research showed that the combination treatment decreased CI/RI induced inflammatory cytokines and oxidative stress, including inhibiting the production of IL-1β, IL-6, TNF-α, decreasing the levels of malondialdehyde (MDA), and increased the activity of </span>superoxide dismutase<span><span> (SOD). In addition, the neuroprotection effect of SAB and MSCs combination was achieved through the regulation of TLR4/NF-κB/MyD88 signaling pathway<span> related proteins, including inhibition the protein levels of TLR4, </span></span>MYD88<span>, p-NF-κB p65, TRAF6-and action of SIRT1 in brain tissues.</span></span></p></div><div><h3>Conclusion</h3><p>The present study indicated that the MSCs and SAB combination treatment had better protective effect against rat ischemic brain injury. The combination of SAB and MSCs may provide a potent and promising strategy for the treatment of ischemic stroke and is worthy for further development.</p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"133 ","pages":"Article 102338"},"PeriodicalIF":2.8,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10240732","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}

{"title":"Aerobic exercise training reduces deep-frying oil-induced apoptosis of hippocampal tissue by reducing oxidative stress in male rats","authors":"Sina Nikbin ,&nbsp;Gita fardad ,&nbsp;Sara Yazdi ,&nbsp;Marzieh Hosseini Bahman ,&nbsp;Parvaneh Ettefagh ,&nbsp;Fatemeh Khalegi ,&nbsp;Mino Molaei ,&nbsp;Kamal Azizbeigi ,&nbsp;Myriam Guerra-Balic ,&nbsp;Joel Montané ,&nbsp;Mehdi Zargani ,&nbsp;Mohammad Ali Azarbayjani","doi":"10.1016/j.jchemneu.2023.102328","DOIUrl":"10.1016/j.jchemneu.2023.102328","url":null,"abstract":"<div><p><span><span><span><span>Deep-frying oil (DFO) contains high amounts of free radicals, and consuming foods prepared with this method causes damage to nervous tissue due to oxidative stress<span> (OS). Since moderate-intensity aerobic exercise training (AT) reduces OS, the current search investigated the effects of AT on OS, apoptosis, and neurogenesis markers in the hippocampal tissue of DFO-fed rats. Eighteen Wistar male rats (200–280 gr) were randomly allocated to a control group fed with normal food (Con-ND), a control group receiving DFO (Con-DFO), and a group receiving DFO-aerobic exercise (EX-DFO) (n = 6 in each). DFO was gavaged for four weeks, five days a week, with a dose of 2 ml. AT included running on a treadmill for four weeks and five sessions per week (40 min per session). The expression of genes B-cell lymphoma 2 (BCL-2), </span></span>Protein X<span> associated with Bcl-2 (BAX), Caspase-3 (Casp-3), and Caspase-9 (Casp-9) was measured by PCR method. The ELISA method was used to calculate levels of </span></span>Superoxide dismutase<span> (SOD) and Catalase (CAT) activity, malondialdehyde (MDA), and Brain-Derived Neurotrophic Factor (BDNF). Also, the expression of the proteins </span></span>Cannabinoid receptor<span> type 1(CB1), Cannabinoid receptor type2 (CB2), Glial fibrillary acidic protein<span> (GFAP), Neuronal nuclei (NeuN), and DNA fragmentation<span> was evaluated by Immunohistochemical and TUNEL staining. DFO feeding led to a significant increase in apoptotic markers, such as BAX, Casp-3, and Casp-9 gene expression, and DNA fragmentation (</span></span></span></span><em>p</em> ≤ 0.05) while decreasing BDNF concentration SOD activity (<em>p</em> ≤ 0.05). AT significantly reduced the BAX, Casp-3, Casp-9, MDA, CB1, GFAP, and DNA fragmentation (<em>p</em> ≤ 0.05). In conclusion, AT can reduce the harmful effects of feeding with DFO on the hippocampal tissue.</p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"133 ","pages":"Article 102328"},"PeriodicalIF":2.8,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10237076","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}

{"title":"Localization and neurochemical identity of alpha1-adrenergic receptor-containing elements in the mouse locus coeruleus","authors":"Zachary N.M. Luyo ,&nbsp;Abigail B. Lawrence ,&nbsp;Theodore G. Stathopoulos ,&nbsp;Darlene A. Mitrano","doi":"10.1016/j.jchemneu.2023.102343","DOIUrl":"10.1016/j.jchemneu.2023.102343","url":null,"abstract":"<div><p><span>The locus coeruleus<span> (LC) is the major source for norepinephrine<span> (NE) in the brain and projects to areas involved in learning and memory, reward, arousal, attention, and autonomic functions related to stress. There are three types of adrenergic receptors<span> that respond to NE: alpha1-, alpha2-, and beta-adrenergic receptors. Previous behavioral studies have shown the alpha1-adrenergic receptor (α1AR) to be present in the LC, however, with conflicting results. For example, it was shown that α1ARs in the LC are involved in some of the motivational effects of stimulation of the medial forebrain bundle<span><span>, which was reduced by α1AR antagonist terazosin. Another study showed that during novelty-induced behavioral activation, the α1AR antagonist </span>prazosin reduced c-fos expression in brain regions known to contain motoric α1ARs, except for the LC, where c-fos expression was enhanced. Despite new research delineating more specific connectivity of the neurons in the LC, and some roles of the adrenergic receptors, the α1ARs have not been localized at the subcellular level. Therefore, in order to gain a greater understanding of the aforementioned studies, we used </span></span></span></span></span>immunohistochemistry<span> at the electron microscopic (EM) level to determine which neuronal or glial elements in the LC express the α1AR. We hypothesized, based on previous work in the ventral periaqueductal gray<span> area, that the α1AR would be found mainly presynaptically in axon terminals<span><span>, and possibly in glial elements. Single labeling immunohistochemistry at the EM revealed that about 40% of labeled elements that contained the α1AR were glial elements, while approximately 50% of the labeled neuronal elements were axon terminals or small unmyelinated axons in the LC. Double labeling immunohistochemistry found the α1AR expressed in GFAP-labeled astrocytes, in both GABAergic and glutamatergic axon terminals, and in a portion of the α1AR dendrites, colocalized with </span>tyrosine hydroxylase (TH, a marker for noradrenergic neurons). This study sheds light on the neuroanatomical framework underlying the effects of NE and pharmaceuticals acting directly or indirectly on α1ARs in the LC.</span></span></span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"133 ","pages":"Article 102343"},"PeriodicalIF":2.8,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41101709","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}

{"title":"Celecoxib attenuates neuroinflammation, reactive astrogliosis and promotes neuroprotection in young rats with experimental hydrocephalus","authors":"Maurício Dutra ,&nbsp;Stephanya Covas da Silva ,&nbsp;Pâmella da Silva Beggiora Marques ,&nbsp;Izadora Oliveira Amaral ,&nbsp;Stephanie Naomi Funo de Souza ,&nbsp;Luiz Antônio Dutra ,&nbsp;Marcelo Volpon Santos ,&nbsp;Hélio Rubens Machado ,&nbsp;Luiza da Silva Lopes","doi":"10.1016/j.jchemneu.2023.102344","DOIUrl":"10.1016/j.jchemneu.2023.102344","url":null,"abstract":"<div><p><span>Hydrocephalus<span> is a neurological condition with altered cerebrospinal fluid flow<span> (CSF). The treatment is surgical and the most commonly used procedure is ventricle-peritoneal shunt. However, not all patients can undergo immediate surgery or achieve complete lesion reversal. Neuroprotective measures are valuable in such cases. It was evaluated whether the use of </span></span></span>celecoxib<span><span>, a selective inhibitor of COX-2, associated or not with ventricular-subcutaneous derivation, could offer benefits to the brain structures affected by experimental hydrocephalus. Seven-day-old male Wistar Hannover rats induced by intracisternal injection of kaolin 15% were used, divided into five groups with ten animals each: intact control (C), untreated hydrocephalus (H), hydrocephalus treated with celecoxib 20 mg/kg intraperitoneal (HTC), hydrocephalus treated with shunt (HTS) and hydrocephalus treated with shunt and celecoxib 20 mg/kg intraperitoneal (HTCS). Celecoxib was administered for 21 consecutive days, starting the day after hydrocephalus induction and continuing until the end of the experimental period. The surgery was performed seven days after inducing hydrocephalus. Multiple assessment methods were used, such as behavioral tests (water maze and open field), histological analysis (hematoxylin and eosin), </span>immunohistochemistry<span><span> (caspase-3, COX-2, and GFAP), and ELISA<span> analysis of GFAP. The results of the behavioral and memory tests indicated that celecoxib improves the neurobehavioral response. The improvement can be attributed to the reduced neuroinflammation (p &lt; 0.05), and </span></span>astrogliosis (p &lt; 0.05) in different brain regions. In conclusion, the results suggest that celecoxib holds great potential as an adjuvant neuroprotective drug for the treatment of experimental hydrocephalus.</span></span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"133 ","pages":"Article 102344"},"PeriodicalIF":2.8,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41132263","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}

{"title":"Cladribine induces apoptosis, neuroinflammation, mitochondrial oxidative stress, tau phosphorylation and Aβ (1–42) pathway in the hippocampus: An in vivo approach","authors":"Khadga Raj Aran ,&nbsp;G.D. Gupta ,&nbsp;Shamsher Singh","doi":"10.1016/j.jchemneu.2023.102340","DOIUrl":"10.1016/j.jchemneu.2023.102340","url":null,"abstract":"<div><p><span><span>Cladribine is a </span>purine nucleoside<span> found to enhance toxic amyloid protein<span><span> and cause memory impairment. Patients following chemotherapy treatment commonly suffer from cognitive deficits more prevalent in the elderly than adults. A previous research study revealed that cladribine has a high affinity to the brain, increases the level of </span>amyloid precursor protein<span>, and results in learning deficits. The study was designed to validate an animal model<span><span> of cladribine administration to rats through mitochondrial oxidative stress, inflammation, apoptosis, tau phosphorylation, and amyloid-β (1–42) accumulation. In this study, all rats were orally given cladribine (0.5 and 1 mg/kg) for 28 days, resulting in impaired spatial memory confirmed by behavioural activity. On day 29, all rats were euthanized, and the hippocampal tissues were isolated and used for the estimation of neuroinflammatory markers, biochemicals parameters (glutathione, </span>catalase, </span></span></span></span></span>lipid peroxidation<span><span><span><span>, and nitrite), amyloid-β (1–42) level, neurotransmitters, and </span>nuclear factor kappa B<span> analysis. Cladribine administration significantly elevated cytokines release, dysbalanced neurotransmitter concentration, and promoted the Aβ accumulation and </span></span>hyperphosphorylation of </span>tau protein. Our study outcome confirmed that cladribine produces cognitive impairment via activation of Nuclear factor kappa B, mitochondrial oxidative stress and dysbalanced of the endogenous antioxidant defence system.</span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"133 ","pages":"Article 102340"},"PeriodicalIF":2.8,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10246071","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}