IBRO Neuroscience Reports最新文献

{"title":"Acupuncture regulates astrocyte neurotoxic polarization to protect blood–brain barrier integrity in delayed thrombolysis through mediating ERK1/2/Cx43 axis","authors":"Zhi-Hui Zhang ,&nbsp;Yu Gu ,&nbsp;Zheng Huang ,&nbsp;Xin-Yu Liu ,&nbsp;Wen-Tao Xu ,&nbsp;Xin-Chang Zhang ,&nbsp;Guang-Xia Ni","doi":"10.1016/j.ibneur.2025.04.005","DOIUrl":"10.1016/j.ibneur.2025.04.005","url":null,"abstract":"<div><h3>Background</h3><div>Thrombolytic therapy remains the standard treatment for acute ischemic stroke. The narrow window for thrombolysis means that delay in treatment worsens brain injury. Astrocytes regulate blood-brain barrier (BBB) integrity and neuroinflammation, yet their neurotoxic polarization exacerbates injury in neuropathological conditions, including ischemic stroke. Delayed recombinant tissue plasminogen activator (rt-PA) thrombolysis disrupts astrocyte homeostasis, further aggravating brain injury. This study investigates whether acupuncture, a key therapy in traditional Chinese medicine, alleviates delayed thrombolysis-induced injury by modulating astrocyte neurotoxic polarization and elucidates the underlying signaling pathway.</div></div><div><h3>Methods</h3><div>A rat model of embolic stroke with delayed rt-PA thrombolysis was established. The effects of infarct volume, BBB integrity, and neuroinflammation of acupuncture were evaluated. Bulk and single-cell transcriptomic analyses were performed to assess astrocyte-specific transcriptional changes. Western blotting, immunofluorescence, and pharmacological inhibition experiments validated molecular mechanisms.</div></div><div><h3>Results</h3><div>Acupuncture reduced infarct volume, improved neurological function, and restored BBB integrity. Transcriptomic analysis revealed dynamic regulation of astrocyte neurotoxic polarization following acupuncture intervention. Further validation experiments demonstrated that acupuncture suppressed the ERK1/2-Cx43 cascade, thereby attenuating astrocyte-mediated neurotoxicity. Pharmacological modulation of this pathway replicated the protective effects of acupuncture, highlighting the role in mitigating astrocyte dysfunction and promoting BBB recovery.</div></div><div><h3>Conclusion</h3><div>Acupuncture mitigates delayed thrombolysis-induced brain injury by modulating astrocyte polarization via the ERK1/2-Cx43 pathway. These findings highlight acupuncture as a potential strategy to enhance thrombolytic therapy safety in ischemic stroke.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 604-618"},"PeriodicalIF":2.0,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143826081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of BMSCs overexpressing intelectin-1 on angiogenesis in rats with cerebral infarction","authors":"Bo Zhu,&nbsp;Kun Guo,&nbsp;Lei Zha,&nbsp;Zhengli Di,&nbsp;Hongwei Zhao,&nbsp;Le Chang,&nbsp;Naibing Gu","doi":"10.1016/j.ibneur.2025.03.012","DOIUrl":"10.1016/j.ibneur.2025.03.012","url":null,"abstract":"<div><h3>Background</h3><div>Cerebral infarction (CI) is a common and frequently occurring acute neurological disease in clinical practice, posing a severe threat to human health. CI results from various causes leading to local cerebral tissue ischemia and hypoxia due to vascular occlusion and impaired blood supply, which in turn leads to tissue necrosis and corresponding clinical manifestations of neurological deficits. However, to date, treatment options for cerebral infarction remain limited. Therefore, it is crucial to rapidly establish collateral circulation to compensate for the occluded vessels and restore blood flow perfusion.</div></div><div><h3>Objective</h3><div>To assess the effect of bone marrow mesenchymal cells transfected with intelectin-1 (Itln-1) gene on the angiogenesis and apoptosis of CI.</div></div><div><h3>Method</h3><div>Lentiviral-mediated transfection of the Itln-1 gene into bone marrow mesenchymal stem cells (BMSCs) was performed, followed by intravenous injection into rats with CI through the tail vein. The volume of the CI, capillary density, and apoptotic cells were detected.</div></div><div><h3>Results</h3><div>With the increase of AKT and eNOS phosphorylation levels, BMSCs with overexpression Itln-1 gene could significantly promote angiogenesis and reduce the infarct volume in the ischemic penumbra. Meanwhile, the ratio of Bcl-2/Bax increased, and apoptotic cells decreased.</div></div><div><h3>Conclusion</h3><div>The overexpression of Itln-1 can effectively promote CI angiogenesis and inhibit cell apoptosis than transplantation of Itln-1 gene or MSCS alone</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 619-626"},"PeriodicalIF":2.0,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143829953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RNF13 variants L311S and L312P associated with developmental epileptic encephalopathy alter dendritic organization in hippocampal neurons","authors":"Valérie C. Cabana ,&nbsp;Marc P. Lussier","doi":"10.1016/j.ibneur.2025.04.004","DOIUrl":"10.1016/j.ibneur.2025.04.004","url":null,"abstract":"<div><div>Developmental and epileptic encephalopathy (DEE) is a group of rare and serious neurological disorders where seizures exacerbate developmental impairment. Recently, genetic mutations in the <em>RNF13</em> gene were reported to cause DEE73. Specifically, two leucines from the ubiquitin E3 ligase RNF13 are converted to serine or proline (L311S and L312P). These mutations are located within a dileucine motif, which impairs RNF13's capacity to interact with AP-3. A second motif allows RNF13 to interact with AP-1 when the dileucine sorting motif is altered. The present study demonstrates that RNF13 variants L311S and L312P are trafficked through an AP-1-dependent pathway in HeLa cells. In cultures of primary rat hippocampal neurons, the protein level of the variants is significantly higher in dendrites than for wild-type protein. L311S and L312P variants alter dendritic components similarly to an RNF13 AP-3-defective binding variant or a dominant negative for RNF13’s ubiquitin ligase activity. Compared to non-transfected neurons, the variants change the distribution of EEA1-positive early endosomes throughout the dendrites. While the WT alters the distribution of lysosomes (Lamp1-positive) in dendrites, the variants only decrease their presence in proximal dendrites. Unlike the variants, RNF13 WT increases the abundance of PSD-95 in distal dendrites. Interestingly, only the variants with altered dileucine motifs decrease the total number of postsynaptic inhibitory protein Gephyrin puncta. This study reports that genetic variants L311S and L312P mainly act as a dominant negative protein. This research provides valuable insights into the dendritic defects that occur when DEE73-associated genetic variants of RNF13 are present.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 559-573"},"PeriodicalIF":2.0,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143816081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Natural polyphenol mangiferin delays neuronal cell senescence by inhibiting neuroinflammation mediated by microglial activation","authors":"Wei Nong ,&nbsp;Xiaoli Chen ,&nbsp;Yixin Chen ,&nbsp;Xueping Feng ,&nbsp;Wen Kong ,&nbsp;Rui Chi ,&nbsp;Li Yan ,&nbsp;Zhiquan Wei","doi":"10.1016/j.ibneur.2025.04.006","DOIUrl":"10.1016/j.ibneur.2025.04.006","url":null,"abstract":"<div><div>Extracellular β-amyloid protein (Aβ) plaques are prominent pathological feature of Alzheimer's disease (AD). Aβ oligomers and plaques induce sustained microglial activation via the adenosine monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR)/interferon regulatory factor 5 (IRF5) signaling pathway. This microglial activation-mediated neuroinflammation can accelerate neuronal cell senescence. Consequently, the regulation of the AMPK/mTOR/IRF5 pathway presents a potential therapeutic target for AD, as it may inhibit neuroinflammation and delay neuronal cell senescence. Mangiferin, a bioactive natural polyphenol extracted from the leaves of <em>Mangifera indica Linn</em>., has garnered significant attention for its anti-inflammatory properties. However, it remains unclear whether mangiferin can modulate the AMPK/mTOR/IRF5 pathway to inhibit microglial activation-mediated neuroinflammation and delay neuronal cell senescence. This study employed both cellular and animal models of neuronal cell senescence to explore the effects of mangiferin on the regulation of the AMPK/mTOR/IRF5 pathway, aiming to inhibit neuroinflammation and delay neuronal cell senescence <em>in vitro</em> and <em>in vivo</em>. Specifically, SH-SY5Y neuroblastoma cells were subjected to a neuroinflammatory microenvironment induced by Aβ1–42-mediated HMC3 microglial activation to induce neuronal cell senescence <em>in vitro</em>. Additionally, SAMP8 accelerated aging mice were utilized as an aging animal model. The results indicate that mangiferin significantly enhances AMPK phosphorylation in microglial cells, inhibits mTOR activation, and downregulates IRF5 expression. These effects collectively suppress microglial activation and markedly reduce the production of pro-inflammatory cytokines by activated microglia. Consequently, there is a decrease in the proportion of neurons arrested in the G0/G1 phase and a reduction in the number of senescence-associated β-galactosidase (SA-β-gal) positive neurons. Furthermore, mangiferin significantly decreases the expression of neuronal cell senescence markers P16Ink4a and P21Cip1. Collectively, these findings suggest that mangiferin effectively regulates the AMPK/mTOR/IRF5 pathway, inhibits neuroinflammation mediated by microglial activation, and delays neuronal cell senescence. This study underscores the potential of mangiferin for the treatment of neuroinflammation and neurodegenerative diseases.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 574-591"},"PeriodicalIF":2.0,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143821262","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anxiety and depression moods is involved in the pathogenesis of postural tachycardia syndrome","authors":"Hongxia Li PhD ,&nbsp;Wei Shao MM ,&nbsp;Lu Gao MM ,&nbsp;Zhenhui Han MM ,&nbsp;Yanyan Xiao MD","doi":"10.1016/j.ibneur.2025.04.001","DOIUrl":"10.1016/j.ibneur.2025.04.001","url":null,"abstract":"<div><h3>Objective</h3><div>To explore the significance of anxiety and depression in children with postural tachycardia syndrome (POTS).</div></div><div><h3>Study design</h3><div>The study enrolled seventy-one children diagnosed as POTS in Beijing Children's Hospital Affiliated to Capital Medical University and Kaifeng Children’s Hospital, aged 13 ± 2 years; The Self-Rating Depression Scale (SDS), the Self-Rating Anxiety Scale (SAS), the Hamilton Depression (HAMD) scale, and the Hamilton Anxiety (HAMA) scale were determined in POTS children. The POTS children were divided into two groups: anxiety/ depression group and non- anxiety / depression group according to the above scales scores. Heart rate (HR), and blood pressure (BP)were monitored by a Dash 2000 Multi-Lead Physiological Monitor.</div></div><div><h3>Results</h3><div>Twenty POTS children consisted of anxiety / depression group. Twelve were girls and eight were boys, with mean age of 14 ± 2 years. The non- anxiety / depression group included fifty-one POTS children aged 12 ± 2 years. Twenty-six were girls and twenty-five were boys. There were no statically differences in weight, gender, systolic blood pressure (SBP), diastolic blood pressure (DBP), and HR in supine. The age and height of anxiety / depression group were higher than that in non- anxiety / depression group. The maxium HR (HRmax) in ten minutes of upright position or tilt, the change of HR from supine to upright (ΔHR), symptom scores in anxiety / depression group were significantly higher than that in non- anxiety / depression group. Four scale scores were correlated with symptom scores and ΔHR.</div></div><div><h3>Conclusions</h3><div>Anxiety and depression emotion might be involved in the pathogenesis of POTS.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 554-558"},"PeriodicalIF":2.0,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143807592","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neural stem cell changes and spatial distribution of AQP4 expression in a fetal goat model of obstructive hydrocephalus","authors":"Xinting Ji ,&nbsp;Qin Zhang ,&nbsp;Yuantao Yang ,&nbsp;Yan Li ,&nbsp;Lihong Li ,&nbsp;Shibin Lin ,&nbsp;Qi Dong ,&nbsp;Zhenling Wan ,&nbsp;Julan Wu ,&nbsp;Jiadong Bao ,&nbsp;Xiaoman Su ,&nbsp;Pengzhi Chen ,&nbsp;Chenyuan Liu ,&nbsp;Weian Song ,&nbsp;Zechen Wang ,&nbsp;Kang Feng ,&nbsp;Xiaoying Li ,&nbsp;Shaojiang Zheng ,&nbsp;Shuo Gu","doi":"10.1016/j.ibneur.2025.03.013","DOIUrl":"10.1016/j.ibneur.2025.03.013","url":null,"abstract":"<div><h3>Background</h3><div>Fetal ventriculomegaly (VM) is a common congenital abnormality with poor outcomes in severe cases, the mechanisms of which include cerebrospinal fluid（CSF）circulation disorders and abnormal neural development. While Aquaporin 4 (AQP4) plays an important role in CSF circulation, its expression in fetal VM has not been fully studied.</div></div><div><h3>Methods</h3><div>Fetal goats at 90–100 days of gestation were divided into experimental (hydrocephalus induced by BioGlue ® injection) and control (untreated cotwin) groups. Ventricular changes were monitored using ultrasound and magnetic resonance imaging <strong>(</strong>MRI). Brain tissues from the periventricular area, subventricular zone, and corpus callosum were collected for immunofluorescence staining to observe neural stem cells, microglia, and astrocytes. AQP4 expression was analyzed by immunofluorescence, western blotting, and real-time quantitative polymerase chain reaction.</div></div><div><h3>Results</h3><div>The ventricles of hydrocephalic goats were significantly enlarged (&gt; mean + 2 SDs) compared with controls. The number of proliferating neural stem cells in the subventricular zone decreased significantly (P &lt; 0.01). Microglial and astrocyte numbers increased significantly in the hydrocephalus group (P &lt; 0.01). AQP4 expression was higher in the corpus callosum, periventricular, and subventricular zones (P &lt; 0.01), with the largest increase in the subventricular zone. AQP4 expression correlated with the increase in IBA1-positive cells (r = 0.979, P = 0.004; r = 0.991, P &lt; 0.001).</div></div><div><h3>Conclusion</h3><div>This study revealed pathological changes following fetal VM as well as the spatial expression of AQP4. These findings provide insights into the pathological changes associated with fetal VM and identify potential therapeutic targets.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 627-637"},"PeriodicalIF":2.0,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143838639","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparative analysis of autonomic nervous system function in patients with postural orthostatic tachycardia syndrome versus a head-up tilt testing-negative cohort","authors":"Jing-Xiu Li MD, PhD ,&nbsp;Xin Qiu MD ,&nbsp;Min Gao MD, PhD","doi":"10.1016/j.ibneur.2025.04.002","DOIUrl":"10.1016/j.ibneur.2025.04.002","url":null,"abstract":"<div><h3>Purpose</h3><div>Postural orthostatic tachycardia syndrome (POTS) is a heterogeneous collection of disorders that correspond to autonomic dysfunction. Until recently, it was mostly unresolved as a clinical issue. Our study investigated autonomic function in patients with POTS.</div></div><div><h3>Methods</h3><div>The research utilizes both pre-test 24-hour Holter monitoring to evaluate heart rate variability (HRV) and instantaneous HRV during the head-up tilt test (HUTT), aiming to discern differences in autonomic nervous system (ANS) function between patients positively diagnosed with POTS and those exhibiting negative HUTT results.</div></div><div><h3>Results</h3><div>The 24-hour Holter results derived from time-domain methods demonstrated that SDNN, SDANN, SDNN index, rMSSD, pNN50, and TINN were significantly elevated in the POTS positive group compared to the HUTT-negative group. Meanwhile, frequency-domain methods revealed that low-frequency and high-frequency were significantly elevated in the POTS-positive group relative to the HUTT-negative group. However, the analysis of instantaneous time-domain and frequency-domain parameters during HUTT, including SDNN, RMSSD, SDSD, PNN50, VLF, LF, and HF, revealed no statistically significant differences.</div></div><div><h3>Conclusion</h3><div>The findings suggest that pre-HUTT HRV, as assessed by 24-hour Holter monitoring, may provide greater clinical relevance in distinguishing between these groups. The study reveals that patients with POTS demonstrate abnormalities in autonomic regulation, characterized by a decrease in sympathetic activity alongside an increase in parasympathetic activity. The dysregulation of autonomic balance likely contributes to the elevated incidence of syncope and presyncope events observed in patients with POTS.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 638-643"},"PeriodicalIF":2.0,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143838684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Preoperative inflammatory pain exacerbates postoperative pain and neurocognitive impairment","authors":"Hui Yuan ,&nbsp;Daofan Sun ,&nbsp;Bo Lu ,&nbsp;Bo Meng ,&nbsp;Rongjun Liu ,&nbsp;Ruichun Wang ,&nbsp;Xiuzhong Xing ,&nbsp;Yiqin Ji ,&nbsp;Qianyu Ming ,&nbsp;Qiusheng Wang ,&nbsp;Junping Chen","doi":"10.1016/j.ibneur.2025.03.010","DOIUrl":"10.1016/j.ibneur.2025.03.010","url":null,"abstract":"<div><h3>Aims</h3><div>Many studies have shown that postoperative pain aggravates perioperative neurocognitive disorder (PND). In this study we aimed to clarify the effect of preoperative inflammatory pain on postoperative pain and cognitive function.</div></div><div><h3>Methods</h3><div>We established the inflammatory pain model by injected complete freund adjuvant (CFA) and the PND model by tibial fracture surgery in 14- month-old C57BL/6 mice. The paw withdrawal threshold and body weight of the mice were measured 7 days before surgery and 3 days after surgery. On the third postoperative day, mice were subjected to behavioral testing or sacrificed to collect brain tissue.</div></div><div><h3>Results</h3><div>The result shows that CFA exacerbated postoperative pain and cognitive dysfunction in mice, enhanced surgery-induced activation of microglia and astrocytes in the hippocampus, and increased surgery-induced the overexpression of IL-1β, IL-6, and TNF-α, as well as aggravated the decreased expression of α7nAChR and the overexpression of HMGB1 in the hippocampus induced by surgery.</div></div><div><h3>Conclusion</h3><div>Our study shows that preoperative inflammatory pain further aggravates postoperative pain and neurocognitive dysfunction in aged rats, and the mechanism may be related to neuroinflammation caused by α7nAChR-mediated CAP dysfunction and high release of HMGB1.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 545-553"},"PeriodicalIF":2.0,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143799147","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":"Distribution of mRNA for the exocytotic calcium sensor, synaptotagmin 9, in mouse brain","authors":"Kwadwo O. Boateng ,&nbsp;Lucian D. Hadford ,&nbsp;Kelly L. Stauch ,&nbsp;Anthony E. Kincaid ,&nbsp;Wallace B. Thoreson","doi":"10.1016/j.ibneur.2025.03.009","DOIUrl":"10.1016/j.ibneur.2025.03.009","url":null,"abstract":"<div><div>The principal Ca^2 + sensors that control fusion of synaptic vesicles are synaptotagmins 1, 2 and 9. Synaptotagmin 9 (Syt9) has received the least attention. We applied RNAscope techniques to coronal sections of adult mouse brain to study the distribution of Syt9 mRNA. Our results showed weak Syt9 mRNA expression in many brain regions but elevated levels in a handful. Regions of strong expression were largely in limbic and sensory areas and included both excitatory and inhibitory neurons. Strongest expression in the brain was in the medial habenula. The interpeduncular nucleus that provides input to medial habenula and amygdala that receives medial habenula output also showed elevated Syt9 mRNA. Sensory regions with strong Syt9 mRNA expression included mitral and periglomerular cells in the olfactory bulb, thalamus, and sensory layers of the superior colliculus. A few putative layer 5 pyramidal cells in somatosensory, auditory and visual cortex were also strongly labeled. Neurons in motor regions including cortex did not generally show elevated expression with the exception of strong labeling of granular and molecular (but not Purkinje) cells in the cerebellum. Hippocampal neurons also showed only weak labeling.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 592-603"},"PeriodicalIF":2.0,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143824424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroprotective effects and mechanisms of the YiQiWenYangSanHan formula on Parkinson's disease mice","authors":"Jinling Liu ,&nbsp;Dong Di ,&nbsp;Suping Sun ,&nbsp;Yan Sun ,&nbsp;Shihan Zhou ,&nbsp;Jing Liu ,&nbsp;Zizhen Qin ,&nbsp;Xinyu Yang ,&nbsp;Xiao Wang ,&nbsp;Zheng Xu ,&nbsp;Boran Zhu ,&nbsp;Haoxin Wu","doi":"10.1016/j.ibneur.2025.03.014","DOIUrl":"10.1016/j.ibneur.2025.03.014","url":null,"abstract":"<div><h3>Background</h3><div>Parkinson's disease (PD) is a complex neurodegenerative disease, which is often treated with obvious side effects such as dopamine replacement therapy. Our team has validated the unique advantages of the traditional Chinese medicine formula, YiQiWenYangSanHan formula (YQWYSHF), through in vitro experiments, confirming its therapeutic potential for PD. Nevertheless, further research and validation are required to fully understand its protective effects and underlying mechanisms against PD.</div></div><div><h3>Aim of this review</h3><div>This study employed an in vivo model to investigate the effects of YQWYSHF on motor impairments, neuroinflammation, and mitochondrial dysfunction in C57BL/6 J mice caused by MPTP.</div></div><div><h3>Materials and methods</h3><div>Sixty C57BL/6 J mice were randomly divided into 5 groups, all groups except the control group were intraperitoneally administered MPTP for 7 days (30 mg/kg). After 4 weeks of drug intragastric treatment, we assessed the dyskinesia of mice treated with different doses of YQWYSHF by behavioral examination. Additionally, immunofluorescence was used to examine the expression of ionized calcium binding adaptor protein 1 (IBA1) and glial fibrillary acidic protein-positive (GFAP) cells. Western blotting was used to assess the expression level of tyrosine hydroxylase (TH), pyrin domain-containing 3 protein (NLRP3), apoptosis-associated speck-like proteins (ASC), cysteine-containing aspartate protease-1 (Caspase-1), interleukin-1β (IL-1β), α-synuclein (α-syn), poly (ADP-ribose) polymerase 1 (PARP1), and poly ADP ribose (PAR). Furthermore, transmission electron microscopy revealed mitochondrial impairment in the neuronal cells of the substantia nigra (SN).</div></div><div><h3>Results</h3><div>YQWYSHF treatment alleviated dyskinesia in a mouse model of PD. Moreover, it increased the TH expression, and could reverse the increase of IBA1, GFAP, NLRP3, ASC, caspase-1,IL-1β, α-syn, PARP1 and PAR proteins induced by MPTP.</div></div><div><h3>Conclusions</h3><div>YQWYSHF protects dopaminergic neurons in PD by attenuating neuroinflammation and mitochondrial dysfunction. This study provides new evidence for the clinical application of traditional Chinese medicine in the treatment of PD.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 528-538"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143759008","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}