IBRO Neuroscience Reports最新文献

{"title":"Neuroprotective effects of alpha-pinene against behavioral deficits in ketamine-induced mice model of schizophrenia: Focusing on oxidative stress status","authors":"Akbar Hajizadeh Moghaddam ,&nbsp;Fatemeh Malekzadeh Estalkhi ,&nbsp;Sedigheh Khanjani Jelodar ,&nbsp;Tabarek Ahmed Hasan ,&nbsp;Soroush Farhadi-Pahnedari ,&nbsp;Mohammad Karimian","doi":"10.1016/j.ibneur.2023.12.012","DOIUrl":"10.1016/j.ibneur.2023.12.012","url":null,"abstract":"<div><p>Schizophrenia (SCZ) is a profound neurological disorder that affects approximately 1% of the global population. Alpha-pinene (α-pinene) is a natural and active monoterpene found in coniferous tree oil, primarily pine, with diverse pharmacological characteristics, including antioxidative, anxiolytic, and antidepressant properties. This research study delves into the neuroprotective effects of α-pinene on oxidative stress, memory deficits, and depressive and anxiety-like behaviors in a ketamine-induced mice model of SCZ using male mice. The mice were randomly divided into six groups: vehicle, control, positive control, ketamine, α-pinene at 50 mg/kg, and α-pinene at 100 mg/kg. Treatment of the ketamine-induced mice model of SCZ with α-pinene yielded significant improvements in depressive and anxiety-like behaviors and cognitive impairments. Furthermore, it significantly elevated glutathione (GSH) levels, total antioxidant capacity (TAC), dopamine levels, catalase (CAT), and superoxide dismutase (SOD) activities while markedly reducing malondialdehyde (MDA) levels. The current study establishes that α-pinene treatment effectively mitigates oxidative damage, cognitive deficits, and depressive and anxiogenic-like behaviors in the brains of ketamine-treated mice. Therefore, α-pinene treatment is an efficacious approach to forestall the neurobehavioral and neurobiochemical adverse effects of the ketamine-induced SCZ model of mice.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2024-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242123022984/pdfft?md5=3a7e8ebe08b1d757d31cc9a69f904dd3&pid=1-s2.0-S2667242123022984-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139393513","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antipsychotic effect of diosgenin in ketamine-induced murine model of schizophrenia: Involvement of oxidative stress and cholinergic transmission","authors":"Benneth Ben-Azu ,&nbsp;Olusegun G. Adebayo ,&nbsp;Aliance Romain Fokoua ,&nbsp;Benjamin Oritsemuelebi ,&nbsp;Emmanuel O. Chidebe ,&nbsp;Chukwuebuka B. Nwogueze ,&nbsp;Lenatababari Kumanwee ,&nbsp;God'swill E. Uyere ,&nbsp;Micheal T. Emuakpeje","doi":"10.1016/j.ibneur.2023.12.008","DOIUrl":"https://doi.org/10.1016/j.ibneur.2023.12.008","url":null,"abstract":"<div><p>A decrease in the levels of antioxidant arsenals exacerbate generation of reactive oxygen/nitrogen species, leading to neurochemical dysfunction, with significant impact on the pathogenesis of psychotic disorders such as schizophrenia. This study examined the preventive and reversal effects of diosgenin, a phyto-steroidal saponin with antioxidant functions in mice treated with ketamine which closely replicates schizophrenia-like symptoms in human and laboratory animals. In the preventive phase, adult mice cohorts were clustered into 5 groups (<em>n</em> = 9). Groups 1 and 2 received saline (10 mL/kg, <em>i.p.),</em> groups 3 and 4 were pretreated with diosgenin (25 and 50 mg/kg), and group 5 received risperidone (0.5 mg/kg) orally for 14 days. Mice in groups 2–5 additionally received a daily dose of ketamine (20 mg/kg, <em>i.p.</em>) or saline (10 mL/kg/day, <em>i.p.</em>). In the reversal phase, mice received intraperitoneal injection of ketamine or saline for 14 consecutive days prior to diosgenin (25 and 50 mg/kg/<em>p.o.</em>/day) and risperidone (0.5 mg/kg/<em>p.o</em>./day) treatment from days 8–14. Mice were assessed for behavioral changes. Oxidative, nitrergic markers, and cholinergic (acetylcholinesterase activity) transmission were examined in the striatum, prefrontal-cortex and hippocampus. Diosgenin prevented and reversed hyperlocomotion, cognitive and social deficits in mice treated with ketamine relative to ketamine groups. The increased acetylcholinesterase, malondialdehyde and nitrite levels produced by ketamine were reduced by diosgenin in the striatum, prefrontal-cortex and hippocampus, but did not reverse striatal nitrite level. Diosgenin increased glutathione, and catalase levels, except for hippocampal catalase activity when compared with ketamine controls. Conclusively, these biochemical changes might be related to the behavioral deficits in ketamine-treated mice, which were prevented and reversed by diosgenin.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2024-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242123022960/pdfft?md5=ac5ff5382981927d22ab5b98683fe104&pid=1-s2.0-S2667242123022960-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139109164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pericyte derivation and transplantation for blood-CNS barrier reconstitution in CNS disorders","authors":"Hyun Woo Kim ,&nbsp;Kenneth Lap Kei Wu ,&nbsp;Kin-Wai Tam ,&nbsp;Ying-Shing Chan ,&nbsp;Daisy Kwok-Yan Shum","doi":"10.1016/j.ibneur.2023.12.007","DOIUrl":"10.1016/j.ibneur.2023.12.007","url":null,"abstract":"<div><p>Disruption of the blood-central nervous system barrier (BCB) is increasingly recognized as a pathological factor in diseases and trauma of the central nervous system. Despite the neuropathological impact, current treatment modalities do not target the BCB; strategies to reconstitute the impaired BCB have been restricted to nutritional and dietary remedies. As an integral cell type in the neurovascular unit, pericytes are crucial to the development, maintenance, and repair of the BCB. As such, pericytes are well poised as cellular agents for reconstitution of the impaired BCB. Here, we summarize recent revelations regarding the role of BCB disruption in diseases and trauma of the central nervous system and highlight how pericytes are harnessed to provide targeted therapeutic effect in each case. This review will also address how recent advances in pericyte derivation strategies can serve to overcome practical hurdles in the clinical use of pericytes.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2024-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242123022947/pdfft?md5=01c4f5ba064fc7c52c2774956a7bbebc&pid=1-s2.0-S2667242123022947-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139395006","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Quantifying morphologies of developing neuronal cells using deep learning with imperfect annotations","authors":"Amir Masoud Nourollah ,&nbsp;Hamid Hassanpour ,&nbsp;Amin Zehtabian","doi":"10.1016/j.ibneur.2023.12.009","DOIUrl":"10.1016/j.ibneur.2023.12.009","url":null,"abstract":"<div><p>The functionality of human intelligence relies on the interaction and health of neurons, hence, quantifying neuronal morphologies can be crucial for investigating the functionality of the human brain. This paper proposes a deep learning (DL) based method for segmenting and quantifying neuronal structures in fluorescence microscopy images of developing neuronal cells cultured in vitro. Compared to the majority of supervised DL-based segmentation methods that heavily rely on creating exact corresponding masks of neuronal structures for the preparation of training samples, the proposed approach allows for imperfect annotation of neurons, as it only requires tracing the centrelines of the neurites. This ability accelerates the preparation of training data by several folds. Our proposed framework is built on a modified version of PSPNet with an EfficientNet backbone pre-trained on the CityScapes dataset. To handle the imperfectness of training samples, we incorporated a weighted combination of two loss functions, namely the Dice loss and Lovász loss functions, into our network. We evaluated the proposed framework and several other state-of-the-art methods on a published dataset of approximately 900 manually quantified cultured mouse neurons. Our results indicate a close correlation between the proposed method and manual quantification in terms of neuron length and the number of branches while demonstrating improved analysis speed. Furthermore, the proposed method achieved high accuracy in neuron segmentation, as evidenced by the evaluation of the neurons’ length and number of branches.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2023-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242123022959/pdfft?md5=5c07bfacaa94592064f32ac9ed611674&pid=1-s2.0-S2667242123022959-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139195212","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recapitulation and investigation of human brain development with neural organoids","authors":"Atsushi Tamada,&nbsp;Keiko Muguruma","doi":"10.1016/j.ibneur.2023.12.006","DOIUrl":"https://doi.org/10.1016/j.ibneur.2023.12.006","url":null,"abstract":"<div><p>Organoids are 3D cultured tissues derived from stem cells that resemble the structure of living organs. Based on the accumulated knowledge of neural development, neural organoids that recapitulate neural tissue have been created by inducing self-organized neural differentiation of stem cells. Neural organoid techniques have been applied to human pluripotent stem cells to differentiate 3D human neural tissues in culture. Various methods have been developed to generate neural tissues of different regions. Currently, neural organoid technology has several significant limitations, which are being overcome in an attempt to create neural organoids that more faithfully recapitulate the living brain. The rapidly advancing neural organoid technology enables the use of living human neural tissue as research material and contributes to our understanding of the development, structure and function of the human nervous system, and is expected to be used to overcome neurological diseases and for regenerative medicine.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2023-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242123022935/pdfft?md5=9238fc54c946653d8cb4b9b8b9226094&pid=1-s2.0-S2667242123022935-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139406237","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Abnormality in GABAergic postsynaptic transmission associated with anxiety in Bronx waltzer mice with an Srrm4 mutation","authors":"Yuka Shirakawa ,&nbsp;Heng Li ,&nbsp;Yuki Inoue ,&nbsp;Hitomi Izumi ,&nbsp;Yoshimi Kaga ,&nbsp;Yu-ichi Goto ,&nbsp;Ken Inoue ,&nbsp;Masumi Inagaki","doi":"10.1016/j.ibneur.2023.12.005","DOIUrl":"https://doi.org/10.1016/j.ibneur.2023.12.005","url":null,"abstract":"<div><p>The homozygous <em>Bronx waltzer</em> (<em>bv</em>) mouse, which shows hearing impairment, also exhibits anxiety accompanied by a reduction in cortical parvalbumin (PV)-positive GABAergic interneurons. Recently, a mutation in splicing factor Ser/Arg repetitive matrix 4 (Srrm4) was found in <em>bv</em> mice. However, the cellular consequences of the <em>Srrm4</em> mutation for anxiety remain unknown. Here, we tested our hypothesis that <em>bv</em> mutant primarily affects interneurons through a cell-intrinsic pathology that leads to a reduction of interneurons and consequently causes anxiety. We found that the anxiety becomes apparent at 6 weeks of age in <em>bv/bv</em> mice. However, in situ hybridization revealed that <em>Srrm4</em> is not expressed in interneurons, but rather dominates in pyramidal neurons. In addition, the PV-positive GABAergic interneurons were not reduced in number in the <em>bv/bv</em> cortex when anxiety became evident. However, electrophysiological abnormality of GABAergic transmission from interneurons was concomitantly present. Pharmacological blockage of GABA_A receptors revealed increased excitability in <em>bv/bv</em> mice, although no gross change occurred in the expression of an <em>Srrm4</em>-downstream gene, <em>Kcc2</em>, which regulates chloride flux upon GABAergic transmission. These findings suggest that the <em>bv</em>-associated <em>Srrm4</em> mutation mainly involves post-synaptic GABAergic transmission in the central nervous system, which may be associated with the anxiety phenotype in <em>bv/bv</em> mice.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2023-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242123022911/pdfft?md5=50b70548445f3fd37f8ded459a484f85&pid=1-s2.0-S2667242123022911-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139090093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Is cerebral small vessel disease a central nervous system interstitial fluidopathy?","authors":"Hafizah Abdul Hamid ,&nbsp;Aqilah Hambali ,&nbsp;Udemeobong Okon ,&nbsp;Che Mohd Nasril Che Mohd Nassir ,&nbsp;Muhammad Zulfadli Mehat ,&nbsp;Anwar Norazit ,&nbsp;Muzaimi Mustapha","doi":"10.1016/j.ibneur.2023.12.004","DOIUrl":"https://doi.org/10.1016/j.ibneur.2023.12.004","url":null,"abstract":"<div><p>A typical anatomical congregate and functionally distinct multicellular cerebrovascular dynamic confer diverse blood-brain barrier (BBB) and microstructural permeabilities to conserve the health of brain parenchymal and its microenvironment. This equanimity presupposes the glymphatic system that governs the flow and clearance of metabolic waste and interstitial fluids (ISF) through venous circulation. Following the introduction of glymphatic system concept, various studies have been carried out on cerebrospinal fluid (CSF) and ISF dynamics. These studies reported that the onset of multiple diseases can be attributed to impairment in the glymphatic system, which is newly referred as central nervous system (CNS) interstitial fluidopathy. One such condition includes cerebral small vessel disease (CSVD) with poorly understood pathomechanisms. CSVD is an umbrella term to describe a chronic progressive disorder affecting the brain microvasculature (or microcirculation) involving small penetrating vessels that supply cerebral white and deep gray matter. This review article proposes CSVD as a form of “CNS interstitial fluidopathy”. Linking CNS interstitial fluidopathy with CSVD will open a better insight pertaining to the perivascular space fluid dynamics in CSVD pathophysiology. This may lead to the development of treatment and therapeutic strategies to ameliorate the pathology and adverse effect of CSVD.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2023-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242123022923/pdfft?md5=64430d18294bdf2e1accc3f125ca1fb9&pid=1-s2.0-S2667242123022923-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139109165","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Citrullinated isomer of myelin basic protein can induce inflammatory responses in astrocytes","authors":"Marika Chikviladze ,&nbsp;Nino Mamulashvili ,&nbsp;Maia Sepashvili ,&nbsp;Nana Narmania ,&nbsp;Jeremy Ramsden ,&nbsp;Lali Shanshiashvili ,&nbsp;David Mikeladze","doi":"10.1016/j.ibneur.2023.12.003","DOIUrl":"10.1016/j.ibneur.2023.12.003","url":null,"abstract":"<div><h3>Purpose</h3><p>During the course of demyelinating inflammatory diseases, myelin-derived proteins, including myelin basic protein(MBP), are secreted into extracellular space. MBP shows extensive post-translational modifications, including deimination/citrullination. Deiminated MBP is structurally less ordered, susceptible to proteolytic attack, and more immunogenic than unmodified MBP. This study investigated the effect of the deiminated/citrullinated isomer of MBP(C8) and the unmodified isomer of MBP(C1) on cultured primary astrocytes.</p></div><div><h3>Methods</h3><p>MBP charge isomers were isolated/purified from bovine brain. Primary astrocyte cultures were prepared from the 2-day-old Wistar rats. For evaluation of glutamate release/uptake a Fluorimetric glutamate assay was used. Expression of peroxisome proliferator-activated receptor-gamma(PPAR-γ), excitatory amino acid transporter 2(EAAT2), the inhibitor of the nuclear factor kappa-B(ikB) and high mobility group-B1(HMGB1) protein were assayed by Western blot analysis. IL-17A expression was determined in cell medium by ELISA.</p></div><div><h3>Results</h3><p>We found that MBP(C8) and MBP(C1) acted differently on the uptake/release of glutamate in astrocytes: C1 increased glutamate uptake and did not change its release, whereas C8 decreased glutamate release but did not change its uptake. Both isomers increased the expression of PPAR-γ and EAAT2 to the same degree. Western blots of cell lysates revealed decreased expression of ikB and increased expression of HMGB1 proteins after treatment of astrocytes by C8. Moreover, C8-treated cells released more nitric oxide and proinflammatory IL-17A than C1-treated cells.</p></div><div><h3>Conclusions</h3><p>These data suggest that the most immunogenic deiminated isomer C8, in parallel to the decreases in glutamate release, elicits an inflammatory response and enhances the secretion of proinflammatory molecules via activation of nuclear factor kappa B(NF-kB).</p></div><div><h3>Summary statement</h3><p>The most modified-citrullinated myelin basic protein charge isomer decreases glutamate release, elicits an inflammatory response and enhances the secretion of proinflammatory molecules via activation of nuclear factor kappa B in astrocytes.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2023-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S266724212302290X/pdfft?md5=c3ec8032f5049e641984d86cb86d4e7f&pid=1-s2.0-S266724212302290X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139023016","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The protective role of prenatal administration of ascorbic acid on autistic-like behavior in a rat model of autism","authors":"Parisa Margedari ,&nbsp;Iran Goudarzi ,&nbsp;Hamid Sepehri","doi":"10.1016/j.ibneur.2023.11.002","DOIUrl":"10.1016/j.ibneur.2023.11.002","url":null,"abstract":"<div><h3>Background</h3><p>Autism is a complicated neurodevelopmental disorder characterized by several behavioral impairments. The pathology of autism is complex and not fully known. Several recent studies have shown alterations in the activities of antioxidant enzymes in autism. Vitamin C is a potent antioxidant that is present in high concentrations in the brain and acts as a neuromodulator. Prefrontal abnormality has been hypothesized to underlie autistic symptoms. The present study investigated the protective effect of prenatally Vitamin C on autistic-like behaviors, oxidative stress status, and histopathological change of prefrontal in valproic acid (VPA) rat model of autism.</p></div><div><h3>Method</h3><p>The model of autism was induced by subcutaneous administration of Valproic acid (600 mg/kg) to pregnant rats at gestational day 12.5. Vitamin C was administered 600 mg/L in drinking water from the 5th day of gestaion (GD5) up to postnatal day 23 (PND23). Thirty-two rat offspring were divided into four groups: Control, Vitamin C, VPA, and Vitamin C + VPA. The offspring were tested for repetitive behaviors and cognitive ability with a Y-maze task and social interaction with a play behavior task on 31st of Postnatal days. Glutathione (GSH), superoxide dismutase (SOD) activity, and the histological change in the prefrontal lobe were assessed at the end of the study. The number of neurons from the left prefrontal lobe was counted in duplicate from slides stained with hematoxylin-eosin.</p></div><div><h3>Results</h3><p>In the Y-maze apparatus, spontaneous alteration significantly decreased in the prenatal VPA treated rats compared to control rats showing autistic-like behavior; pre and postnatal Vitamin C treatment increased the alternation indicated benefit effect of Vitamin C. Prenatal VPA treatment impaired play behavior such as sniffing, grooming and darting. Vitamin C treatment attenuated the problems in male offspring social behavior. Histological examination showed an increase in the number of cells in the prefrontal cortex of valproic acid offspring rats compared to other groups. Moreover, prenatal VPA decreased antioxidant enzyme activities in the cortex (PFC) attenuated by Vitamin C administration.</p></div><div><h3>Conclusion</h3><p>The present study showed that valproic acid induced oxidative stress and neural changes in the prefrontal lobe when administered prenatally which in turn may cause the development of some autistic-like behaviors, and vitamin C may reduce this symptom with its antioxidant effects</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2023-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242123022807/pdfft?md5=7a7930af4debc3367c89175c07093269&pid=1-s2.0-S2667242123022807-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139018567","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ferulic acid via attenuation of oxidative stress and neuro-immune response utilizes antinociceptive effect in mouse model of formalin test","authors":"Shima Balali-Dehkordi ,&nbsp;Saeid Habibian-Dehkordi ,&nbsp;Hossein Amini-Khoei ,&nbsp;Rahil Mohajerian","doi":"10.1016/j.ibneur.2023.12.001","DOIUrl":"https://doi.org/10.1016/j.ibneur.2023.12.001","url":null,"abstract":"<div><h3>Introduction</h3><p>Plenty evidences suggests that neuroinflammation and oxidative stress augmented the neural sensitivity specifying that neuro-immune response is involved in the pathophysiology of pain. Ferulic acid (FA), a natural antioxidant found in various fruits, has various pharmacological properties. The purpose of the current study was to assess the antinociceptive effect of FA in a mouse model of formalin test with focus on its anti-neuroinflammatory and antioxidative stress effects.</p></div><div><h3>Methods</h3><p>The injection of FA (40 mg/kg), piroxicam (2 mg/kg), and saline (0.9% NaCl) (1 ml/kg) was done intraperitoneally and after one hour, formalin injected into the plantar surface of the hind paw of mice. Then pain behavior was documented during 60 min. Then mice were euthanized and prefrontal cortex (PFC) samples were taken. Malondialdehyde (MDA) level, antioxidant capacity and expression of inflammatory genes, counting tumor necrosis factor (TNF-) and interleukine 1 (IL-1) evaluated in the PFC.</p></div><div><h3>Results</h3><p>exhibited that FA declined the pain behavior following injection of formalin. Besides, FA significantly diminished the MDA level and increased the antioxidant capacity in the PFC. We revealed that FA diminished the expression of TNF-α and IL-1β genes in the PFC.</p></div><div><h3>Conclusion</h3><p>We conclude that FA exerted antinociceptive effects in the formalin test in mice, at least partially, by reducing oxidative stress and neuroimmune response in the PFC.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2023-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242123022893/pdfft?md5=4892bde747f06a182c2a450ac16f1e66&pid=1-s2.0-S2667242123022893-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138739130","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}