Acta neurobiologiae experimentalis最新文献

{"title":"Altered granulocyte count and erythrocyte measures in middle-aged, healthy carriers of APOE and PICALM risk genes for Alzheimer's disease.","authors":"Patrycja Dzianok,&nbsp;Ewa Kublik","doi":"10.55782/ane-2023-012","DOIUrl":"https://doi.org/10.55782/ane-2023-012","url":null,"abstract":"<p><p>APOE‑ε4 genotype (apolipoprotein E, epsilon 4) is the strongest genetic risk factor for Alzheimer's disease (AD). Despite years of research, it is still not known how it contributes to dementia development. APOE has been implicated in many AD pathology mechanisms, like Aβ clearance, brain metabolism, changes within microglia and other glial functions and inflammatory processes. In fact, immunological/inflammatory processes are recently discussed as an important factor in Alzheimer's development and granulocyte profiles changes are reported in patients. However, the exact link between the immune system and risk‑genes is unknown. In particular, it is not known whether and how they interact throughout the lifetime, before the disease onset. The aim of the study was to investigate the relationship between granulocyte count and the APOE/PICALM genes in healthy individuals with an increased genetic risk of AD. An exploratory analysis regarding other blood cells was also conducted. Blood samples were collected from 77 healthy middle‑aged (50-63 years old) participants, who were also asked to complete a health and life‑style questionnaires. Groups with different AD risk‑genes were compared. Differences in granulocyte profiles were found in healthy carriers of AD risk‑genes who had slightly elevated eosinophil levels as compared to non-risk carriers. An exploratory analysis showed some alteration in mean corpuscular hemoglobin content and concentration (MCH/MCHC) levels between risk‑carriers subgroups and non-risk carriers. No other differences in blood count or lipoprotein profile were found between healthy APOE/PICALM risk‑carriers and non-risk carriers. Longitudinal studies will reveal if and how those changes contribute to the development of AD pathology.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 2","pages":"127-139"},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9866990","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 role of neurofilament light chain in COVID‑19: A potential prognostic biomarker.","authors":"Arash Heidari,&nbsp;Nima Rezaei","doi":"10.55782/ane-2023-011","DOIUrl":"https://doi.org/10.55782/ane-2023-011","url":null,"abstract":"<p><p>Coronavirus disease 2019 (COVID‑19) is an unprecedented global health concern that was declared a pandemic in March 2020. Although primarily recognized by respiratory symptoms, growing evidence suggested the causal relationship between the infection with the disease agent, namely severe acute respiratory coronavirus 2 (SARS‑CoV‑2), and neurological manifestations. Given that the virus‑induced neurological involvement is associated with a poorer prognosis, persistent neurological sequelae, and a more severe form of the disease, efforts have been made to introduce a biomarker to recognize neurological abnormalities early in the course of the disease. Studies indicate a significantly higher concentration of neurofilament light chain (NFL) in cerebrospinal fluid or blood of COVID‑19 patients versus adjusted controls. It has also been reported that COVID‑19 patients suffering from the severe form of the disease had higher NFL levels than patients with mild to moderate forms. Moreover, elevated NFL levels at hospital admission in patients who did not present primarily with neurological expressions could predict the emergence of neurological symptoms during the hospital stay. The early recognition of neurological abnormalities using the NFL biomarker could lead to escalated medical care limiting the progression of SARS‑CoV‑2‑induced central nervous system pathogenesis, resulting in a significant amelioration in disease outcome. Nevertheless, NFL assessment integrated with the evaluation of other neurodegenerative biomarkers and factors indicating disease prognosis could provide a more comprehensive estimate of disease prognosis and the extent of neurological involvement.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 2","pages":"111-126"},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9866991","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":"Fasudil alleviates cerebral ischemia‑reperfusion injury by inhibiting inflammation and improving neurotrophic factor expression in rats.","authors":"Min-Fang Guo, Hui-Yu Zhang, Pei-Jun Zhang, Yi-Jin Zhao, Jing-Wen Yu, Tao Meng, Meng-Di Li, Na Li, Cun-Gen Ma, Li-Juan Song, Jie-Zhong Yu","doi":"10.55782/ane-2023-010","DOIUrl":"10.55782/ane-2023-010","url":null,"abstract":"<p><p>The Rho kinase inhibitor fasudil exerts neuroprotective effects. We previously showed that fasudil can regulate M1/M2 microglia polarization and inhibit neuroinflammation. Here, the therapeutic effect of fasudil on cerebral ischemia‑reperfusion (I/R) injury was investigated using the middle cerebral artery occlusion and reperfusion (MCAO/R) model in Sprague‑Dawley rats. The effect of fasudil on the phenotype of microglia and neurotrophic factors in the I/R brain and its potential molecular mechanism was also explored. It was found that fasudil ameliorated neurological deficits, neuronal apoptosis, and inflammatory response in rats with cerebral I/R injury. Fasudil also promoted the polarization of microglia into the M2 phenotype, in turn promoting the secretion of neurotrophic factors. Furthermore, fasudil significantly inhibited the expression of TLR4 and NF‑κB. These findings suggest that fasudil could inhibit the neuroinflammatory response and reduce brain injury after I/R injury by regulating the shift of microglia from an inflammatory M1 phenotype to an anti‑inflammatory M2 phenotype, which may be related to the regulation of the TLR4/ NF‑κB signal pathway.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 1","pages":"97-110"},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9378665","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":"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":"The effect of nicotine on antidepressant and anxiolytic responses induced by citalopram and citicoline in mice.","authors":"Fatemeh Khakpai,&nbsp;Mohammad-Reza Zarrindast","doi":"10.55782/ane-2023-017","DOIUrl":"https://doi.org/10.55782/ane-2023-017","url":null,"abstract":"<p><p>The effect of nicotine on both anxiety and depression has been broadly studied. Moreover, citalopram and citicoline play a role in the modulation of anxiety and depression. This study was designed to examine the effects of nicotine on the antidepressant and anxiolytic responses induced by citalopram and citicoline in mice. Anxiety‑ and depression‑related behaviors were assessed with the elevated plus maze and forced swim test, respectively. The results showed that subcutaneous administration of nicotine decreased open‑arm time (OAT) and open‑arm entries (OAE) but increased immobility time, suggesting anxiogenic‑like and depressive‑like effects. Intraperitoneal administration of citalopram increased OAT but decreased immobility time, indicating that citalopram induced anxiolytic‑like and antidepressant‑like responses. Additionally, an injection of citicoline increased OAE but decreased immobility time, revealing anxiolytic‑like and antidepressant‑like effects. Interestingly, the subthreshold dose of nicotine potentiated the citalopram and citicoline effects on OAT and immobility time, which revealed anxiolytic‑like and antidepressant‑like behaviors. Locomotor activity was not significantly changed by any doses of the drugs. In conclusion, these findings suggest that interactions between nicotine and citalopram or citicoline occur upon induction of anxiolytic and antidepressant responses in mice.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 2","pages":"194-202"},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9875742","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":"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}