Journal of chemical neuroanatomy最新文献

{"title":"Gelatin/polyethylene glycol-loaded magnesium hydroxide nanocomposite to attenuate acetylcholinesterase, neurotoxicity, and activation of GPR55 protein in rat models of Alzheimer's disease","authors":"Manickam Rajkumar ,&nbsp;Sundarraj Navaneethakrishnan ,&nbsp;Sundarapandian Muthukumar ,&nbsp;Ramasundaram Thangaraj ,&nbsp;Magudeeswaran Sivanandam ,&nbsp;Karuppaiya Vimala ,&nbsp;Soundarapandian Kannan","doi":"10.1016/j.jchemneu.2023.102337","DOIUrl":"10.1016/j.jchemneu.2023.102337","url":null,"abstract":"<div><p><span><span>Alzheimer's disease<span> (AD) is a neurodegenerative disease marked by mitochondrial dysfunction, amyloid-β (Aβ) aggregation, and neuronal cell loss. G-protein-coupled receptor 55 (GPR55) has been used as a promising target for </span></span>insulin receptors<span> in diabetes therapy, but GPR55's<span> role in AD is still unidentified. Gelatin (GE) and polyethylene glycol<span> (PEG) polymeric hydrogels are commonly used in the drug delivery system. Therefore, the aim of the present study was the preparation of magnesium hydroxide nanocomposite using </span></span></span></span><span><em>Clitoria ternatea</em></span> (CT) flower extract, GE, and PEG (GE/PEG/Mg(OH)₂NCs) by the green precipitation method. The synthesized GE/PEG/Mg(OH)₂<span><span>NCs were used to determine the effect of GPR55 activation of intracerebroventricular administration on streptozotocin<span> (ICV-STC)-induced cholinergic dysfunction, oxidative stress, neuroinflammation, and </span></span>cognitive deficits. The GE/PEG/Mg(OH)</span>₂<span>NCs were administered following bilateral ICV-STC administration (3 mg/kg) in experimental rats. Neurobehavioral assessments were performed using a Morris water maze<span><span> (MWM) and a passive avoidance test (PA). Cholinergic and </span>antioxidant activity<span><span>, oxidative stress, and mitochondrial complex activity were estimated in the cortex and hippocampus through </span>biochemical analysis<span>. Inflammatory markers (TNF-α, IL-6, and IL-1β) were determined using the ELISA method. Our study results demonstrated that the GE/PEG/Mg(OH)</span></span></span></span>₂NCs treatment significantly improved spatial and non-spatial memory functions in behavioral studies. Moreover, the treatment with GE/PEG/Mg(OH)₂<span><span>NCs group significantly attenuated cholinergic dysfunction, oxidative stress, and inflammatory markers, and also highly improved anti-oxidant activity (GSH, SOD, </span>CAT<span>, and GPx) in the cortex and hippocampus regions. The western blot<span> results suggest the activation of the GPR55 protein expression through GE/PEG/Mg(OH)</span></span></span>₂<span><span>NCs. The histopathological studies showed clear cytoplasm and healthy neurons, effectively promoting neuronal activity. Furthermore, the </span>molecular docking<span> results demonstrated the binding affinity<span> and potential interactions of the compounds with the AChE enzyme. In conclusion, the GE/PEG/Mg(OH)</span></span></span>₂<span>NCs treated groups showed reduced neurotoxicity and have the potential as a therapeutic agent to effectively target AD.</span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"133 ","pages":"Article 102337"},"PeriodicalIF":2.8,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10240734","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":"Dendritic reorganization in the hippocampus, anterior temporal lobe, and frontal neocortex of lithium-pilocarpine induced Status Epilepticus (SE)","authors":"Vivek Dubey ,&nbsp;Avishek Roy ,&nbsp;Aparna Banerjee Dixit ,&nbsp;Manjari Tripathi ,&nbsp;Shivam Pandey ,&nbsp;Suman Jain ,&nbsp;P.Sarat Chandra ,&nbsp;Jyotirmoy Banerjee","doi":"10.1016/j.jchemneu.2023.102329","DOIUrl":"10.1016/j.jchemneu.2023.102329","url":null,"abstract":"<div><p><span><span>Status Epilepticus<span><span><span> (SE) is a distributed network disorder, which involves the hippocampus and extra-hippocampal structures. </span>Epileptogenesis<span> in SE is tightly associated with neurogenesis, plastic changes and </span></span>neural network<span> reorganization facilitating hyper-excitability. On the other hand, dendritic spines are known to be the excitatory synapse in the brain. Therefore, dendritic spine dynamics could play an intricate role in these network alterations. However, the exact reason behind these structural changes in SE are elusive. In the present study, we have investigated the aforementioned hypothesis in the lithium-pilocarpine treated rat model of SE. We have examined cytoarchitectural and morphological changes using hematoxylin-eosin and Golgi-Cox </span></span></span>staining in three different brain regions viz. CA1 pyramidal layer of the dorsal hippocampus, layer V pyramidal neurons of anterior temporal lobe (ATL), and frontal neocortex of the same animals. We observed macrostructural and layer-wise alteration of the pyramidal layer mainly in the hippocampus and ATL of SE rats, which is associated with sclerosis in the hippocampus. Sholl analysis exhibited partial dendritic plasticity in apical and basal dendrites of </span>pyramidal cells as compared to the saline-treated weight-/age-matched control group. These findings indicate that region-specific alterations in dendritogenesis may contribute to the development of independent epileptogenic networks in the hippocampus, ATL, and frontal neocortex of SE rats.</p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"133 ","pages":"Article 102329"},"PeriodicalIF":2.8,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10231223","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":"GABA-immunoreactive neurons in the Central Nervous System of the viviparous teleost Poecilia sphenops","authors":"Achyutham Hotha,&nbsp;C.B. Ganesh","doi":"10.1016/j.jchemneu.2023.102339","DOIUrl":"10.1016/j.jchemneu.2023.102339","url":null,"abstract":"<div><p><span><span>Gamma-aminobutyric acid (GABA) functions as the primary inhibitory neurotransmitter within the </span>central nervous system<span> (CNS) of vertebrates. In this study, we examined the distribution pattern of GABA-immunoreactive (GABA-ir) cells and fibres in the CNS of the viviparous teleost </span></span><em>Poecilia sphenops</em><span><span><span><span> using immunofluorescence method. GABA immunoreactivity<span> was seen in the glomerular, mitral, and granular layers of the olfactory bulbs, as well as in most parts of the dorsal and ventral telencephalon. The </span></span>preoptic area<span><span> consisted of a small cluster of GABA-ir cells, whereas extensively labelled GABA-ir neurons were observed in the hypothalamic areas, including the paraventricular organ, tuberal hypothalamus, nucleus recessus lateralis, nucleus recessus posterioris, and inferior lobes. In the thalamus, GABA-positive neurons were only found in the ventral thalamic and central posterior thalamic nuclei, whereas the dorsal part of the nucleus pretectalis periventricularis consisted of a few GABA-ir cells. GABA-immunoreactivity was extensively seen in the alar and basal subdivisions of the midbrain, whereas in the </span>rhombencephalon, GABA-ir cells and fibres were found in the </span></span>cerebellum, motor nucleus of glossopharyngeal and vagal nerves, nucleus commissuralis of Cajal, and </span>reticular formation. In the spinal cord, GABA-ir cells and fibres were observed in the dorsal horn, ventral horn, and around the central canal. Overall, the extensive distribution of GABA-ir cells and fibres throughout the CNS suggests several roles for GABA, including the neuroendocrine, viscerosensory, and somatosensory functions, for the first time in a viviparous teleost.</span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"133 ","pages":"Article 102339"},"PeriodicalIF":2.8,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10287681","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":"Aripiprazole attenuates the medial prefrontal cortex morphological and biochemical alterations in rats with neonatal ventral hippocampus lesion","authors":"Gabriel D. Flores-Gómez ,&nbsp;David Javier Apam-Castillejos ,&nbsp;Ismael Juárez-Díaz ,&nbsp;Estefania Fuentes-Medel ,&nbsp;Alfonso Díaz ,&nbsp;Hiram Tendilla-Beltrán ,&nbsp;Gonzalo Flores","doi":"10.1016/j.jchemneu.2023.102316","DOIUrl":"10.1016/j.jchemneu.2023.102316","url":null,"abstract":"<div><p><span><span>Schizophrenia<span><span> is a neurodevelopmental disorder characterized by a loss of </span>dendritic spines in the medial prefrontal cortex (mPFC). Multiple subclinical and clinical studies have evidenced the ability of </span></span>antipsychotics<span><span> to improve neuroplasticity<span><span>. In this study, it was evaluated the effect of the atypical antipsychotic </span>aripiprazole<span> (ARI) on the behavioral and mPFC neuronal disturbances of rats with neonatal ventral hippocampus lesion (nVHL), which is a heuristic developmental model relevant to the study of schizophrenia. ARI attenuated open field hyperlocomotion in the rats with nVHL. Also, ARI ameliorated structural neuroplasticity disturbances of the mPFC layer 3 </span></span></span>pyramidal cells<span><span>, but not in the layer 5 neurons. These effects can be associated with the ARI capability of increasing brain-derived neurotrophic factor (BDNF) levels. Moreover, in the animals with nVHL, ARI attenuated the immunoreactivity for some oxidative stress-related molecules such as the </span>nitric oxide synthase 2 (NOS-2), 3-nitrotyrosine (3-NT), and </span></span></span>cyclooxygenase<span><span> 2 (COX-2), as well as the reactive astrogliosis in the mPFC. These results contribute to current knowledge about the neurotrophic, anti-inflammatory, and antioxidant properties of antipsychotics which may be contributing to their clinical effects and envision promising therapeutic targets for the </span>treatment of schizophrenia.</span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"132 ","pages":"Article 102316"},"PeriodicalIF":2.8,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10628975","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 effects of myricitrin and chebulinic acid on the rat hippocampus exposed to gamma radiation: A stereological, histochemical and biochemical study","authors":"Sümeyye Gümüş Uzun ,&nbsp;Berrin Zuhal Altunkaynak ,&nbsp;Işınsu Alkan","doi":"10.1016/j.jchemneu.2023.102305","DOIUrl":"10.1016/j.jchemneu.2023.102305","url":null,"abstract":"<div><h3>Aim</h3><p>Gamma radiation, a form of ionizing radiation, is used in many different areas, especially in the health field and in the treatment of cancer. However, gamma radiation used for therapeutic purposes also has numerous harmful effects on human health. This study was planned to investigate the impacts of exposure to gamma radiation on the hippocampal area and the preventive effects of myricitrin and chebulinic acid against that damage.</p></div><div><h3>Material and method</h3><p>Thirty-six male Wistar albino rats were randomly divided into six groups. The control group was exposed to no treatment. The chebulinic acid and myricitrin groups were injected with the relevant drug at a dosage of 0.033 mg/kg) (vehicle; normal saline) per day. The gamma groups were placed in a plexiglass test setup with their heads positioned close to the source. The subjects were exposed to radiation with a mixed source containing radioactive Cs-137 and Co-60 isotopes obtained from Ondokuz Mayıs University Physics Department Nuclear Physics Laboratory for 1 h. Gamma radiation was applied 16 mGy for one hour per day for 10 days. The gamma radiation+chebulinic acid and the gamma radiation myricitrin groups also received 0.033 mg/kg per day of these drugs via injection. Immediately after the experimental procedure, all animals were subjected to behavioural tests, and perfused brain tissues were analyzed using stereological methods.</p></div><div><h3>Results</h3><p>Stereological analysis showed that gamma radiation caused a decrease in the numbers of neurons in the hippocampal area (p &lt; 0.01; One-way ANOVA) and that chebulinic acid and myricitrin reduced this decrease (p &lt; 0.01; One-way ANOVA). Decreases in learning and memory capacity were detected in behavioural tests in rats from the Gamma group.</p></div><div><h3>Conclusion</h3><p>The study findings showed that that the adverse health effects of Gamma radiation can be ameliorated using myricitrin and chebulinic acid. Myricitrin was more effective in terms of cell proliferation<span> and defence against oxidative stress<span> than chebulinic acid, and exhibited a more neuroprotective effect. However, more detailed analyses should be performed before using either antioxidant for therapeutic purposes.</span></span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"132 ","pages":"Article 102305"},"PeriodicalIF":2.8,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10283996","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":"Lacosamide exhibits neuroprotective effects in a rat model of Parkinson's disease","authors":"Burcin Bilal ,&nbsp;Mehmet Kirazlar ,&nbsp;Mumin Alper Erdogan ,&nbsp;Gurkan Yigitturk ,&nbsp;Oytun Erbas","doi":"10.1016/j.jchemneu.2023.102311","DOIUrl":"10.1016/j.jchemneu.2023.102311","url":null,"abstract":"<div><h3>Background</h3><p>Parkinson's disease<span><span><span> (PD) is a chronic and progressive neurodegenerative disorder that primarily affects the motor system. Although there are several treatments available to alleviate PD symptoms, there is currently no cure for the disease. </span>Lacosamide<span>, an anti-epileptic drug, has shown promising results in preclinical studies as a potential </span></span>neuroprotective agent for PD. In this study, we aimed to investigate the neuroprotective effect of lacosamide in a murine model of PD.</span></p></div><div><h3>Methods</h3><p>Twenty-one adult male rats were randomly divided into the following three groups (<em>n</em><span><span><span> = 7): 1 group received stereotaxical infusion of dimethyl sulfoxide (vehicle, group 1), and the others received stereotaxical infusion of </span>rotenone (groups 2 and 3). The apomorphine-induced rotation test was applied to the rats after 10 days. Thereafter, group 2 was administered isotonic saline, whereas group 3 was administered lacosamide (20 mg/kg,i.p.) for 28 days. Apomorphine-induced rotation tests were performed to assess the effect of lacosamide on motor function. In addition, </span>immunohistochemistry<span><span><span> and biochemistry<span> were used to assess the dopaminergic neuron loss in the </span></span>substantia nigra and MDA, TNF-α and </span>HVA levels, respectively.</span></span></p></div><div><h3>Results</h3><p>In rats with Parkinson's disease induced by rotenone, levels of malondialdehyde and TNF-α significantly increased and HVA levels decreased, whereas in mice treated with lacosamide, levels of malondialdehyde and TNF-α significantly decreased and HVA levels increased. The apomorphine-induced rotation test scores of lacosamide-treated mice were lower compared with the untreated group. Furthermore, treatment with lacosamide significantly mitigated the degeneration of dopaminergic projections within the striatum originating from the substantia nigra and increased tyrosine hydroxylase (TH) immunofluorescence, indicative of preserved dopaminergic neuronal function.</p></div><div><h3>Conclusion</h3><p>In conclusion, our study provides evidence that lacosamide has a neuroprotective effect on the rat model of PD. Further studies are required to investigate the underlying mechanisms and evaluate the potential clinical use of lacosamide as a neuroprotective agent for PD.</p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"132 ","pages":"Article 102311"},"PeriodicalIF":2.8,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10273291","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":"Cleavage of semaphorin 4 C interferes with the neuroprotective effect of the semaphorin 4 C/Plexin B2 pathway on experimental intracerebral hemorrhage in rats","authors":"Dong Li ,&nbsp;Xiang Li Sr ,&nbsp;Jiahe Wang ,&nbsp;Haiying Li ,&nbsp;Haitao Shen ,&nbsp;Xiang Xu ,&nbsp;Gang Chen","doi":"10.1016/j.jchemneu.2023.102318","DOIUrl":"10.1016/j.jchemneu.2023.102318","url":null,"abstract":"<div><p><span>Semaphorin<span><span> 4 C (SEMA4C) and its cognate receptor Plexin B2 are important regulators of </span>axon guidance<span><span> and are involved in many neurological diseases, in which SEMA4C acts not only as a ligand (\"forward\" mode) but also as a signaling receptor (\"reverse\" mode). However, the role of SEMA4C/Plexin B2 in </span>intracerebral hemorrhage (ICH) remains unclear. In this study, ICH in adult male Sprague-Dawley rats was induced by </span></span></span>autologous blood injection<span> in the right basal ganglia. In vitro, cultured primary neurons were subjected to OxyHb<span><span><span> to imitate ICH injury. Recombinant SEMA4C (rSEMA4C) and overexpressing lentiviruses encoding full-length SEMA4C or secretory SEMA4C (sSEMA4C) were administered to rats by intraventricular injection. First, we found that elevated levels of sSEMA4C in the cerebrospinal fluid (CSF) of clinical patients were associated with poor prognosis. Both SEMA4C and sSEMA4C were increased in brain tissue around the </span>hematoma after ICH in rats. Overexpression of SEMA4C attenuated </span>neuronal apoptosis<span>, neurosis<span>, and neurologic impairment after ICH. However, treatment with rSEMA4C or sSEMA4C overexpression exacerbated neuronal injury. In addition, when treated with SEMA4C overexpression, the forward mode downstream protein RhoA and the reverse mode downstream ID1/3 transcriptional factors of SEMA4C/Plexin B2 signaling were all activated. Nevertheless, when exposed to rSEMA4C or sSEMA4C overexpression, only the forward mode was activated. Thus, sSEMA4C may be a novel molecular biomarker to predict the prognosis of patients with ICH, and the prevention of SEMA4C cleavage is expected to be a promising therapeutic target.</span></span></span></span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"132 ","pages":"Article 102318"},"PeriodicalIF":2.8,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10284502","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":"Silymarin pretreatment protects against ethanol-induced memory impairment: Biochemical and histopathological evidence","authors":"A. Jabbari ,&nbsp;B. Alani ,&nbsp;A. Arjmand ,&nbsp;T. Mazoochi ,&nbsp;N. Kheiripour ,&nbsp;A. Ardjmand","doi":"10.1016/j.jchemneu.2023.102310","DOIUrl":"10.1016/j.jchemneu.2023.102310","url":null,"abstract":"<div><h3>Background</h3><p><span><span>Ethanol (Eth.) abuse induces memory impairment. Oxidative damage and apoptosis are considered the likely causes of memory impairment. Silymarin (Sil.) is a </span>flavonoid isolated from the plant </span><em>Silymarin marianum</em><span><span> (milk thistle). While studies have reported the neuroprotective effect of Sil. against </span>neurodegenerative processes, the precise mechanism of action of Sil. in Eth.-induced memory impairment remains unclear.</span></p></div><div><h3>Methods</h3><p>Twenty-eight rats were equally divided into four groups: Control (saline 1 ml/rat); Sil. (200 mg/kg for 30 days); Eth. (2 g/kg/day for 30 days); and Sil. + Eth. Behavioral tests including inhibitory avoidance and open field were used to investigate memory and locomotion. Brain antioxidant parameters, including catalase<span>, superoxide dismutase<span>, total antioxidant capacity and total thiol group, plus oxidative parameters, including malondialdehyde and total oxidant status, followed by hippocampal apoptosis (Bax/Bcl2, cleaved caspase) and histopathological changes were evaluated in the groups.</span></span></p></div><div><h3>Results</h3><p>While the administration of Eth. impaired memory, Sil. significantly reversed Eth-induced memory deficits. Eth. administration also augmented brain oxidative and hippocampal apoptosis parameters. In contrast, a marked reduction in brain antioxidant and anti-apoptotic parameters was observed in the Eth. group. At the tissue level, hippocampal sections from Eth.-treated animals revealed severe neuronal damage. The administration of Sil. to Eth.-treated rats remarkably alleviated all the said Eth.-induced biochemical and histopathological effects. On the contrary, Sil. alone did not change the behavior and biochemical/molecular parameters.</p></div><div><h3>Conclusion</h3><p>The memory-enhancing effect of Sil. in Eth.-induced demented rats may be partly mediated by the augmented antioxidant effects and amelioration of apoptotic and histopathological changes.</p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"132 ","pages":"Article 102310"},"PeriodicalIF":2.8,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10272816","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":"10-dehydrogingerdione amends tramadol-elicited neurotransmitters disturbance and apoptosis in the brain of male rats by repleting non-enzymatic antioxidants","authors":"Mohamed M. ELseweidy ,&nbsp;Sousou I. Ali ,&nbsp;Laila Sabik ,&nbsp;Salma E. Sewilam","doi":"10.1016/j.jchemneu.2023.102302","DOIUrl":"10.1016/j.jchemneu.2023.102302","url":null,"abstract":"<div><p><span><span><span><span>Tramadol is analgesic medication to relief acute and chronic pain, referred to as alternative to opioid drugs however its abuse or overdosage may resulted in neuronal toxicity. This is attributed to severe fluctuations of neurotransmitters pattern along with cerebral inflammation and oxidative damage. Present work was undertaken to illustrate the cytoprotective effect of 10-dehydrogingerdione (10-DHGD) on the brain tissues of experimental rats due to Tramadol intake and its underlying mechanism. 24 male </span>wistar rats were randomized into 4 equal groups. Group (1), received tramadol in a dose level 20 mg/kg intrapertioneal (i.p) daily for 30 days and referred to Tramadol group. Group (2), received both of 10-DHGD (10 mg/kg, orally) one hour before tramadol intake (dose as mentioned before) daily for 30 days. Group (3) received 10-DHGD only (10 mg/kg, orally) and daily for 30 days. Group (4), received no drugs and referred to control group for comparison. Tramadol significantly reduced </span>Norepinephrin<span> (NE), dopamine, serotonin and glutathione (reduced) contents of </span></span>Cerebral cortex. </span>lipid peroxidation<span><span>, nuclear factor kappa B (NFkB), </span>inducible nitric oxide synthase<span><span> (INOS) levels and caspase-3 immunoreactivity<span> showed however significant increase. Of note, 10-DHGD significantly increased neurotransmitters, glutathione contents while Malondialdehyde (MDA), Nitric oxide (NO), NFkB, INOS additionally caspase-3 immunoexpression showed significant decrease i.e counteracted to certain extent tramadol effect. These findings may refer to the cytoprotective potential of 10-DHGD against the </span></span>neurotoxicity exerted by tramadol intake, most probably mediated via enhancement of endogenous antioxidants system.</span></span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"132 ","pages":"Article 102302"},"PeriodicalIF":2.8,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10644964","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":"TRIM6 silencing for inhibiting growth and angiogenesis of gliomas by regulating VEGFA","authors":"Xin Liu ,&nbsp;Junling Zhao ,&nbsp;PengFei Dong ,&nbsp;Xinyuan Du ,&nbsp;Wenpeng Lu ,&nbsp;Yan Feng ,&nbsp;Liqun Wang","doi":"10.1016/j.jchemneu.2023.102291","DOIUrl":"10.1016/j.jchemneu.2023.102291","url":null,"abstract":"<div><p>Gliomas are the highest prevalent primary central nervous system (CNS) cancers with poor overall survival rate. There is an urgent need to conduct more research into molecular therapies<span><span><span> targeting critical elements of gliomas. This study herein targeted to assess the impact of tripartite motif protein<span> 6 (TRIM6) on gliomas. Using public databases, we found the increased TRIM6 expression in tissues of glioma which was linked with worst overall survival. Silencing TRIM6 promoted glioma cell proliferation, migration and </span></span>angiogenesis, suggesting the promoting effects of TRIM6 on gliomas. Knockdown of TRIM6 expression downregulated the expression levels of Forkhead box M1 (FOXM1) and </span>vascular endothelial growth factor A (VEGFA) in glioma cells. Afterwards, impact of TRIM6 on VEGFA expression was regulated by FOXM1. VEGFA overexpression reversed the decreased abilities of glioma cell proliferation, migration and angiogenesis caused by silencing TRIM6. Furthermore, we also found that TRIM6 promoted the growth of gliomas in the xenograft mouse model. In summary, the expression of TRIM6 was increased which was related to poor prognosis of glioma patients. TRIM6 promoted glioma cell proliferation, migration and angiogenesis through the FOXM1-VEGFA pathway. Therefore, TRIM6 carries capacity to be explored as a novel therapeutic target in clinical.</span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"132 ","pages":"Article 102291"},"PeriodicalIF":2.8,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10271792","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}