Acta neurobiologiae experimentalis最新文献

{"title":"Bilateral subdiaphragmatic vagotomy modulates the peripheral met‑enkephalin and striatal monoamine responses to peripheral inflammation in rat.","authors":"Anna Teresa Kobrzycka,&nbsp;Adrian Mateusz Stankiewicz,&nbsp;Paweł Napora,&nbsp;Krystyna Pierzchała-Koziec,&nbsp;Marek Wieczorek","doi":"10.55782/ane-2023-009","DOIUrl":"https://doi.org/10.55782/ane-2023-009","url":null,"abstract":"<p><p>In the central nervous system, long‑term effects of a vagotomy include disturbance of monoaminergic activity of the limbic system. Since low vagal activity is observed in major depression and autism spectrum disorder, the study aimed to determine whether animals fully recovered after subdiaphragmatic vagotomy demonstrates neurochemical indicators of altered well‑being and social component of sickness behavior. Bilateral vagotomy or sham surgery was performed in adult rats. After one month of recovery, rats were challenged with lipopolysaccharide or vehicle to determine the role of central signaling upon sickness. Striatal monoamines and met‑enkephalin concentrations were evaluated using HPLC and RIA methods. We also defined a concentration of immune‑derived plasma met‑enkephalin to establish a long‑term effect of vagotomy on peripheral analgesic mechanisms. The data indicate that 30 days after vagotomy procedure, striatal dopaminergic, serotoninergic, and enkephalinergic neurochemistry was altered, both under physiological and inflammatory conditions. Vagotomy prevented inflammation‑induced increases of plasma met‑enkephalin - an opioid analgesic. Our data suggest that in a long perspective, vagotomized rats may be more sensitive to pain and social stimuli during peripheral inflammation.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 1","pages":"84-96"},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9378664","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":"Effects of varied‑intensity endurance exercise training on oxidative and antioxidant factors in the liver of rats with valproic acid‑induced autism.","authors":"Farzad Mirzavandi,&nbsp;Nazanin Sabet,&nbsp;Azadeh Aminzadeh,&nbsp;Mahmoodreza Heidari,&nbsp;Fatemeh Pouya,&nbsp;Amirhossein Moslemizadeh,&nbsp;Ali Saeidpour Parizi,&nbsp;Hamideh Bashiri","doi":"10.55782/ane-2023-003","DOIUrl":"https://doi.org/10.55782/ane-2023-003","url":null,"abstract":"<p><p>Autism spectrum disorders are complex behavioral disorders that can be caused by exposure to valproic acid (VPA) during pregnancy. A therapeutic role for exercise training has been reported in many neurological diseases and problems, including autism. We aimed to evaluate various intensities of endurance exercise training and investigate its effects on oxidative and antioxidant factors in the liver of young males in a rat model of autism. Female rats were divided into a treatment (autism) and a control group. The autism group received VPA intraperitoneally on day 12.5 of pregnancy and the control pregnant females received saline. On the 30th day post‑birth, a social interaction test was performed on the offspring to confirm autistic‑like behavior. Offspring were divided into three subgroups: no exercise, mild exercise training, and moderate exercise training. Then the oxidative index of malondialdehyde (MDA) and the antioxidant indices of superoxide dismutase (SOD), total antioxidant capacity (TAC), and catalase in liver tissue were examined. The results of this study showed that both indices of sociability and social novelty decreased in the autism group. MDA levels in the liver of the autistic group increased, and moderate exercise training was shown to reduce the levels. Catalase and SOD activity as well as TAC levels decreased in the autism group, and moderate‑intensity exercise training was shown to increase the values. Parameters of hepatic oxidative stress were altered in VPA‑induced autism, and moderate‑intensity endurance exercise training was demonstrated to have beneficial effects on hepatic oxidative stress factors by modul ating the antioxidant/oxidant ratio.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 1","pages":"25-33"},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9384491","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":"Peripheral and cerebral inflammation induced by repeated anesthesia and surgery do not cause impairment of learning and memory in middle‑aged mice.","authors":"Jian Lu,&nbsp;Xiaoyan Tao,&nbsp;Hongyu Dai,&nbsp;Sunan Gao,&nbsp;Hongmei Zhou","doi":"10.55782/ane-2023-005","DOIUrl":"https://doi.org/10.55782/ane-2023-005","url":null,"abstract":"<p><p>Postoperative cognitive dysfunction is a postoperative complication of the central nervous system that reduces quality of life and increases mortality in perioperative patients, especially among elderly patients. Many studies have shown that the incidence of postoperative cognitive impairment in adults induced by one‑time anesthesia and surgery is very low, while multiple experiences of anesthesia and surgery can induce cognitive impairment in the developing brain. However, the effect of multiple experiences of anesthesia and surgery on cognitive function over a short period in middle‑aged mice, i.e., 6 to 8 months old, remains unclear. In this study, we explored whether the cognitive function of mice aged 6-8 months is impaired after multiple operations. Middle‑aged mice (6 to 8 months old) healthy male C57BL/6 mice underwent exploratory laparotomy under isoflurane anesthesia. Morris water maze testing was performed after the operations. Blood and brain samples were collected at 6 h, 24 h, and 48 h after the operations. Serum IL‑6, IL‑1, and S‑100β concentrations were detected by ELISA. The expressions of ChAT, AChE, and Aβ in the hippocampus were measured by western blot. Up‑regulation of Iba1 and GFAP, respectively, indicated activation of microglia and astrocytes in the hippocampus. Expression of Iba1 and GFAP was examined by immunofluorescence. The present results revealed that serum IL‑6, IL‑1β, and S‑100β concentrations were enhanced after multiple instances of anesthesia and surgery, and microglia and astrocytes in the hippocampus were activated. However, learning and memory were not impaired in the middle‑aged mice by multiple experiences of anesthesia and surgery. There were no changes in ChAT, AChE, and Aβ in the hippocampus after multiple experiences of anesthesia/surgery. Taken together, we suggest that although multiple anesthesia/surgery procedures can induce peripheral inflammation, neuroinflammation, and transient cerebral injury, it is insufficient to impair learning and memory in middle‑aged mice.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 1","pages":"45-56"},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9384495","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":"Minocycline protects against neuronal mitochondrial dysfunction and cognition impairment.","authors":"Majid Motaghinejad,&nbsp;Manijeh Motevalian,&nbsp;Luis Ulloa,&nbsp;Neda Kaviani,&nbsp;Emre Hamurtekin","doi":"10.55782/ane-2023-008","DOIUrl":"https://doi.org/10.55782/ane-2023-008","url":null,"abstract":"<p><p>The potential of minocycline to protect against methylphenidate‑induced neurodegeneration has been extensively reported in the literature but the mechanism of action is still unknown. This study aims to determine the role of mitochondrial chain enzymes and redox homeostasis on the neuroprotective effects of minocycline in methylphenidate‑induced neurodegeneration. Wistar adult male rats were randomly assigned to the seven experimental groups: Group 1 received saline solution; Group 2 received methylphenidate (10 mg/kg, i.p.); Groups 3, 4, 5, and 6 received methylphenidate and minocycline for 21 days; Group 7 received minocycline alone. Cognition was evaluated with the Morris water maze test. Activity of the hippocampal mitochondrial quadruple complexes I, II, III and IV, mitochondrial membrane potential, adenosine triphosphate (ATP) levels, total antioxidant capacity, and reactive oxygen species were determined. Treatment with minocycline inhibited methylphenidate‑induced cognitive dysfunction. Minocycline treatment increased mitochondrial quadruple complex activities, mitochondrial membrane potential, total antioxidant capacity, and ATP levels in the dentate gyrus and cornu ammonis‑1 (CA1) areas of the hippocampus. Minocycline is likely to confer neuroprotection against methylphenidate‑induced neurodegeneration and cognition impairment by regulating mitochondrial activity and oxidative stress.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 1","pages":"71-83"},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9384493","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":"A synergistic analgesic effect of morphine in combination with the CB1 receptor agonist, ACPA, in normal, hypothyroid, and hyperthyroid male rats.","authors":"Mohammad-Reza Zarrindast,&nbsp;Fatemeh Khakpai","doi":"10.55782/ane-2023-014","DOIUrl":"https://doi.org/10.55782/ane-2023-014","url":null,"abstract":"<p><p>Both cannabinoid and opioid receptors are involved in pain behavior. The administration of morphine and cannabis in rats has been shown to decrease thyroid weight and thyroid‑stimulating hormone (TSH) levels. We hypothesized that the third ventricle, due to its adjacency to the hypothalamus, is involved in the modulation of hypothalamic‑pituitary‑thyroid axis activity and descending pain pathways. The present study examined the effect of intra‑third ventricle administration of morphine and cannabis agents on the modulation of pain behavior in normal, hypothyroid (increased serum TSH), and hyperthyroid (decreased serum TSH) rats using the tail‑flick test. The results indicated that intra‑third ventricle injection of AM251 (CB1 receptor antagonist) caused hyperalgesia, while intra‑third ventricle administration of ACPA (CB1 receptor agonist) and morphine produced analgesia in normal, hypothyroid, and hyperthyroid rats. A non‑effective dose of morphine (0.5 μg/rat) did not attenuate hyperalgesia induced by an effective dose of AM251. Co‑injection of ACPA and morphine into the third ventricle induced anti‑nociceptive effect in normal, hypothyroid, and hyperthyroid rats. An isobolographic analysis demonstrated a synergistic effect between ACPA and morphine in the production of the anti‑nociceptive effect. Consequently, the third ventricle may modulate pain behavior induced by cannabinoid and opioid receptors via descending pain pathways in normal, hypothyroid, and hyperthyroid rats.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 2","pages":"154-170"},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9875740","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":"Comparative effects of the alcoholic extract of Terminalia chebula and crocin on stress‑induced anxiety‑like behavior and memory impairment in male rats.","authors":"Gila Pirzad Jahromi,&nbsp;Zohreh Jangravi,&nbsp;Mohammadmehdi Hadipour,&nbsp;Hossein Shirvani,&nbsp;Mohammad Reza Afarinesh,&nbsp;Gholam Hossein Meftahi","doi":"10.55782/ane-2023-016","DOIUrl":"https://doi.org/10.55782/ane-2023-016","url":null,"abstract":"<p><p>Crocin and Terminalia chebula (T. chebula) were proven to have neuroprotective effects. In this study, we evaluated the preventive effects of crocin and alcoholic extract of the T. chebula alone and in combination to examine their efficacy against chronic restraint stress (CRS)‑induced cognitive impairment, anxiety‑like behaviors, hippocampal synaptic plasticity deficit as well as neuronal arborization damage in the hippocampal CA1 neurons. Over 14 consecutive days, animals received crocin, T. chebula, or their combination (5 min before CRS). The elevated plus‑maze results showed that crocin and T. chebula alone and in combination treatment significantly increased the time spent in open arms, percentage of open arm entries, and head dipping as compared with the CRS group. Barnes maze results showed that administration of crocin and T. chebula alone and their combination significantly improves spatial memory indicators such as distance traveled, latency time to achieving the target hole, and the number of errors when compared to the CRS group. These learning deficits in CRS animals correlated with a reduction of long-term potentiation (LTP) in hippocampal CA1 synapses, which both T. chebula and crocin treatment improved field excitatory postsynaptic potentials (fEPSP) amplitude and fEPSP slope reduction induced by CRS. Golgi‑Cox staining showed that T. chebula and crocin treatment increased the number of dendrites and soma arbors in the CA1 neurons compared with the CRS group. Our results suggest that both T. chebula and crocin attenuated CRS‑induced anxiety‑like behaviors, memory impairment, and synaptic plasticity loss in hippocampal CA1 neurons. We found no significant difference between single treatments of T. chebula or crocin and their combination in protecting CRS‑induced anxiety‑like behaviors, memory impairment, and synaptic plasticity loss in hippocampal CA1 neurons.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 2","pages":"179-193"},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9875741","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":"Effect of milnacipran on brain‑derived neurotrophic factor and oxidative stress biomarkers in patients of major depressive disorder.","authors":"Rachna Gupta,&nbsp;Rupanwita Ghosh,&nbsp;Manjeet S Bhatia,&nbsp;A K Tripathi,&nbsp;Lalit K Gupta","doi":"10.55782/ane-2023-006","DOIUrl":"https://doi.org/10.55782/ane-2023-006","url":null,"abstract":"<p><p>Emerging hypotheses in the pathophysiology of major depressive disorder (MDD) suggest important role of neurotrophic factors and oxidative stress. This study assessed the effect of milnacipran (a dual serotonin‑noradrenaline reuptake inhibitor) on brain‑derived neurotrophic factor (BDNF) and oxidative stress biomarkers i.e., malondialdehyde (MDA), glutathione‑s‑ transferase (GST) and glutathione reductase (GR) in patients of MDD. Thirty patients (aged 18 to 60 years) with MDD diagnosed by DSM‑IV criteria, with Hamilton Depression Rating scale (HAM‑D) score ≥ 14 were included in the study. Patients were given milnacipran in the doses of 50‑100 mg once daily. Patients were followed up for 12 weeks. HAM‑D score at the start of treatment was 17.8±1.7 which significantly reduced to 8.9±3.1 at 12 weeks of treatment. In responders, the plasma BDNF levels increased significantly at 12 weeks post treatment. There was no significant change in the pre‑ and post‑treatment values of oxidative stress parameters (MDA, GST and GR) after 12 week treatment. Milnacipran is effective and well tolerated in MDD patients, and its therapeutic response is associated with an increase in plasma BDNF levels. However, milnacipran did not affect oxidative stress biomarkers.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 1","pages":"57-62"},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9384492","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":"Hyperammonemia induced gut microbiota dysbiosis and motor coordination disturbances in mice: new insight into gut‑brain axis involvement in hepatic encephalopathy.","authors":"Aimrane Abdelmohcine,&nbsp;Souad El Amine,&nbsp;Karima Warda,&nbsp;Soraia El Baz,&nbsp;Manal Khanouchi,&nbsp;Bilal El-Mansoury,&nbsp;Mustapha Agnaou,&nbsp;Kamal Smimih,&nbsp;Nadia Zouhairi,&nbsp;Hicham Chatoui,&nbsp;Ahmed Draoui,&nbsp;Fatimazahra Saad,&nbsp;Elamiri My Ahmed,&nbsp;Abdessalam Ferssiwi,&nbsp;Abdelali Bitar,&nbsp;Arumugam R Jayakumar,&nbsp;Naima Fdil,&nbsp;Omar El Hiba","doi":"10.55782/ane-2023-018","DOIUrl":"https://doi.org/10.55782/ane-2023-018","url":null,"abstract":"<p><p>Hepatic encephalopathy (HE) is a neuropsychiatric hepatic‑induced syndrome in which several factors are involved in promoting brain perturbations, with ammonia being the primary factor. Motor impairment, incoordination, and gut dysbiosis are some of the well‑known symptoms of HE. Nevertheless, the link between the direct effect of hyperammonemia and associated gut dysbiosis in the pathogenesis of HE is not well established. Thus, this work aimed to assess motor function in hyperammonemia and gut dysbiosis in mice. Twenty‑eight Swiss mice were distributed into three groups: two‑week and four‑week hyperammonemia groups were fed with an ammonia‑rich diet (20% w/w), and the control group was pair‑fed with a standard diet. Motor performance in the three groups was measured through a battery of motor tests, namely the rotarod, parallel bars, beam walk, and static bars. Microbial analysis was then carried out on the intestine of the studied mice. The result showed motor impairments in both hyperammonemia groups. Qualitative and quantitative microbiological analysis revealed decreased bacterial load, diversity, and ratios of both aerobic and facultative anaerobic bacteria, following two and four weeks of ammonia supplementation. Moreover, the Shannon diversity index revealed a time‑dependent cutback of gut bacterial diversity in a treatment‑time‑dependent manner, with the presence of only Enterobacteriaceae, Streptococcaceae, and Enterococcaceaeat at four weeks. The data showed that ammonia‑induced motor coordination deficits may develop through direct and indirect pathways acting on the gut‑brain axis.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 2","pages":"203-215"},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9875743","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":"Assessment of the relationship between Val66Met BDNF polymorphism and the effectiveness of gait rehabilitation in children and adolescents with cerebral palsy.","authors":"Bartosz Bagrowski, Marta Czapracka, J. Krásný, Michal Prendecki, J. Dorszewska, M. Jóźwiak","doi":"10.55782/ane-2022-001","DOIUrl":"https://doi.org/10.55782/ane-2022-001","url":null,"abstract":"Cerebral palsy (CP) is associated with the non‑progressive damage of upper motor neurons, which is manifested by a variety of symptoms, particularly motor and functional deficits. During the rehabilitation of patients with CP, attention is paid to improving mobility which can have a significant impact on the child's development. The effectiveness of rehabilitation depends on the plasticity of the nervous system, which may be genetically determined. Of importance are the various polymorphisms of the brain derived neurotrophic factor (BDNF) gene. It has been shown that the Val/Val genotype may predispose children to greater improvements in function and its maintenance. However, subjects with the Met allele showed a reduced tendency to improve their motor functions but had significantly better results on indirect tests assessing gait function. Fifty subjects with CP participated in this study. They were divided into two groups by genotype and examined on their rehabilitation progress in terms of improved gait function. The results correlated with other studies describing the relationship between the BDNF genotype and learning motor functions in CP, and with numerous studies on the relationship between BDNF genotype and neuroplasticity in stroke patients. This research provides a basis for the identification of genetic biomarkers in patients with CP which can be used to predict the effects of rehabilitation therapy and help with the development of personalized treatments.","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"82 1 1","pages":"1-11"},"PeriodicalIF":1.4,"publicationDate":"2022-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46325261","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":"Apelin‑13 ameliorates LPS‑induced BV‑2 microglia inflammatory response through promoting autophagy and inhibiting H3K9ac enrichment of TNF‑α and IL‑6 promoter.","authors":"Qingling Peng, Jiahui Zhou, Zhewei Xu, Qiancheng Zhao, Zhi-yue Li, Qun Zhao","doi":"10.55782/ane‑2022‑006","DOIUrl":"https://doi.org/10.55782/ane‑2022‑006","url":null,"abstract":"Microglia is activated and polarized to pro‑inflammatory M1 phenotype or anti‑inflammatory M2 phenotype in neuroinflammation. Apelin‑13 exerts protective properties against neuroinflammation in several neurological disorders. We aimed to investigate whether apelin‑13 played a protective role on BV‑2 microglia and explore its underlying mechanisms. Lipopolysaccharide (LPS)‑stimulated BV‑2 microglia cells were treated with apelin‑13. Microglia activation was evaluated by immunofluorescence with F‑actin. Western blot was performed to measure the expression of autophagy associated proteins. CD16/32 and CD206 were detected to assess microglia polarization by western blot and flow cytometry. qRT‑PCR was utilized to measure inducible nitric oxide synthase (iNOS), arginase‑1 (Arg‑1), interleukin‑10 (IL‑10), interleukin‑6 (IL‑6) and tumor necrosis factor‑alpha (TNF‑α). Histone H3 acetyl lysine 9 (H3K9ac) enrichment of TNF‑α and IL‑6 promoter was detected by ChIP. We discovered that apelin‑13 impacted the actin cytoskeleton, recovering the control phenotype following LPS exposure. Apelin‑13 improved autophagy‑mediated microglia polarization towards M2 phenotype to alleviate inflammatory response in LPS‑stimulated cells. Autophagy flux inhibitor chloroquine antagonized these effects of apelin‑13 on LPS‑stimulated cells. Besides, apelin‑13 decreased the enrichment of H3K9ac at the promoter region of TNF‑α and IL‑6 to inhibit inflammatory response, which was reversed by histone deacetylase antagonist valproate. Taken together, apelin‑13 alleviated inflammation via facilitating microglia M2 polarization due to autophagy promotion, and inhibiting H3K9ac enrichment on promoter regions of TNF‑α and IL‑6.","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"82 1 1","pages":"65-76"},"PeriodicalIF":1.4,"publicationDate":"2022-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70810338","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}