Brain Research Bulletin最新文献_第7页

Induction of tau pathology and motor dysfunction in mice by urinary exosomes from progressive supranuclear palsy patients 进行性核上性麻痹患者尿液外泌体诱导小鼠的 tau 病理学和运动功能障碍。

IF 3.5 3区医学

Brain Research Bulletin Pub Date : 2024-08-05 DOI: 10.1016/j.brainresbull.2024.111046

{"title":"Induction of tau pathology and motor dysfunction in mice by urinary exosomes from progressive supranuclear palsy patients","authors":"","doi":"10.1016/j.brainresbull.2024.111046","DOIUrl":"10.1016/j.brainresbull.2024.111046","url":null,"abstract":"<div><h3>Background</h3><p>Progressive supranuclear palsy (PSP) is characterized by the presence of hyperphosphorylated and misfolded tau aggregates in neurons and glia. Recent studies have illuminated the prion-like cell-to-cell propagation of tau via exosomes. Recognizing the potential significance of excretion through urine as a crucial pathway for eliminating pathological tau from the central nervous system, this study aimed to investigate whether exosomes derived from the urine of PSP-Richardson's syndrome (PSP-RS) patients can elicit tau pathology and PSP-like symptoms in mice.</p></div><div><h3>Methods</h3><p>Urinary exosomes obtained from PSP-RS patients and normal controls (NCs) were stereotactically injected into the bilateral globus pallidus of mouse brains. Behavioral analyses were conducted every 3 months post-injection. After 6 months, mice were sacrificed for pathological evaluation.</p></div><div><h3>Results</h3><p>Elevated levels of phosphorylated tau and neural cell markers were observed in urinary exosomes from PSP-RS patients compared to NCs. At the 6-month mark post-injection, tau inclusions were evident in the brains of mice receiving urinary exosomes from PSP-RS patients, with widespread distribution in both injection sites and distant brain regions (cortex, hippocampus, and substantia nigra). Tau pathology manifested in neurons and astrocytes. Moreover, mice injected with urinary exosomes from PSP-RS patients exhibited impaired motor coordination and balance, mirroring PSP motor symptoms.</p></div><div><h3>Conclusion</h3><p>Our findings indicate that urinary exosomes from PSP-RS patients can induce tau pathology and trigger PSP-like motor symptoms in mice. This leads to the hypothesis that exosomes may play a role in the pathogenesis of PSP.</p></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0361923024001795/pdfft?md5=8e6b1d32f4fc767732e1e6c5f91ef8f3&pid=1-s2.0-S0361923024001795-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141900978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Simvastatin alleviates glymphatic system damage via the VEGF-C/VEGFR3/PI3K-Akt pathway after experimental intracerebral hemorrhage 辛伐他汀通过血管内皮生长因子-C/血管内皮生长因子受体3/PI3K-Akt途径减轻实验性脑出血后的甘油系统损伤。

IF 3.5 3区医学

Brain Research Bulletin Pub Date : 2024-08-05 DOI: 10.1016/j.brainresbull.2024.111045

{"title":"Simvastatin alleviates glymphatic system damage via the VEGF-C/VEGFR3/PI3K-Akt pathway after experimental intracerebral hemorrhage","authors":"","doi":"10.1016/j.brainresbull.2024.111045","DOIUrl":"10.1016/j.brainresbull.2024.111045","url":null,"abstract":"<div><p>Current clinical practice primarily relies on surgical intervention to remove hematomas in patients with intracerebral hemorrhage (ICH), given the lack of effective drug therapies. Previous research indicates that simvastatin (SIM) may enhance hematoma absorption and resolution in the acute phase of ICH, though the precise mechanisms remain unclear. Recent findings have highlighted the glymphatic system (GS) as a crucial component in intracranial cerebrospinal fluid circulation, playing a significant role in hematoma clearance post-ICH. This study investigates the link between SIM efficacy in hematoma resolution and the GS. Our experimental results show that SIM alleviates GS damage in ICH-induced rats, resulting in improved outcomes such as reduced brain edema, neuronal apoptosis, and degeneration. Further analysis reveals that SIM's effects are mediated through the VEGF-C/VEGFR3/PI3K-Akt pathway. This study advances our understanding of SIM's mechanism in promoting intracranial hematoma clearance and underscores the potential of targeting the GS for ICH treatment.</p></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0361923024001783/pdfft?md5=989abe34e7eb6a130320551ce5db50ef&pid=1-s2.0-S0361923024001783-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141888535","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The role of D1-like dopamine receptors within the ventral tegmental area in the cannabidiol’s inhibitory effects on the methamphetamine-induced conditioned place preference in rats 大麻二酚对甲基苯丙胺诱导的大鼠条件性位置偏好的抑制作用中，腹侧被盖区的 D1 类多巴胺受体所起的作用。

IF 3.5 3区医学

Brain Research Bulletin Pub Date : 2024-08-03 DOI: 10.1016/j.brainresbull.2024.111038

{"title":"The role of D1-like dopamine receptors within the ventral tegmental area in the cannabidiol’s inhibitory effects on the methamphetamine-induced conditioned place preference in rats","authors":"","doi":"10.1016/j.brainresbull.2024.111038","DOIUrl":"10.1016/j.brainresbull.2024.111038","url":null,"abstract":"<div><p>Cannabidiol (CBD) is a non-psychoactive drug extracted from marijuana. It is well established that CBD attenuates the reinforcing effects of drugs of abuse, although its mechanism of action is not fully understood. The current study tries to clarify the role of D1-like dopamine receptors (D1R) in the ventral tegmental area (VTA) in the inhibitory effects of the CBD on the acquisition and expression of methamphetamine (METH)-conditioned place preference (CPP). In the CPP training, adult male Wistar rats were conditioned with subcutaneous administration of METH (1 mg/kg) for five days. Three groups of animals were treated with multiple doses of SCH23390 (as a D1R antagonist; 0.25, 1, and 4 μg/0.3 μl saline) in the VTA, respectively, before intracerebroventricular (ICV) injection of CBD (10 μg/5 μl DMSO) in the acquisition phase. In the second experiment of the study, rats received SCH23390 in the VTA before ICV administration of CBD (50 μg/5 μl DMSO) in the expression of METH CPP. Here, the current study demonstrated that CBD inhibits the acquisition and expression of METH CPP, while microinjection of D1R antagonists (1 and 4 μg) into the VTA significantly reduced CBD’s suppressive effect on the acquisition and expression of METH place preference. Furthermore, this research demonstrated that either SCH23390 or CBD alone does not lead to place preference in the CPP paradigm. Based on these data, this study suggests that pharmacological manipulations of D1R may alter the CBD’s effect on METH-conditioned preference.</p></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0361923024001710/pdfft?md5=a866c70f25452c2da012923611160377&pid=1-s2.0-S0361923024001710-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141888536","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Silymarin ameliorates motor function and averts neuroinflammation-induced cell death in the rat model of Huntington’s disease 水飞蓟素能改善亨廷顿症大鼠模型的运动功能，并避免神经炎症引起的细胞死亡。

IF 3.5 3区医学

Brain Research Bulletin Pub Date : 2024-07-31 DOI: 10.1016/j.brainresbull.2024.111039

{"title":"Silymarin ameliorates motor function and averts neuroinflammation-induced cell death in the rat model of Huntington’s disease","authors":"","doi":"10.1016/j.brainresbull.2024.111039","DOIUrl":"10.1016/j.brainresbull.2024.111039","url":null,"abstract":"<div><p>Huntington's disease (HD) is a scarce neurodegenerative disorder defined by chorea (unusual involuntary movements), behavioral presentations, psychiatric features, and cognitive deterioration. Although the precise pathogenic mechanism behind HD has not yet been identified, the most widely acknowledged pathways include excitotoxicity, mitochondrial malfunction, neuroinflammation, neurochemical imbalance, oxidative stress, and apoptosis HD has no efficient therapy. Current medications have drawbacks. Silymarin, a compound made up of standardized extracts obtained from the seeds of the Silybum marianum and polyphenolic flavonolignan, is utilized in therapeutic settings to treat a variety of experimental disorders in animals. Silymarin's key pharmacological activities include anti-cancer, hepatoprotection, antioxidant, cardioprotection, and anti-inflammatory. It also has no adverse side effects on people or animals. The current study aims to provide Silymarin's neuro-pharmacological activities or therapeutic qualities in HD. In this study, Thirty-six male Sprague-Dawley rats (200–220 g, 8 weeks) at the initial of the study were used. Silymarin solution (100 mg/Kg) was administered by oral gavage for 21 days to ameliorate neural damage in rats injected with 3-nitropropionicacid (3-NP) in a preliminary rat model of HD. The results showed that administration of silymarin to HD rats reduced gliosis, improved motor coordination and muscle activity, and increased striatal volume and the number of neurons and glial cells. Our results suggest that silymarin provides a protective environment for nerve cells and can have beneficial effects against the harmful effects of HD.</p></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0361923024001722/pdfft?md5=234224f5c2f39afa364193a5ad47f4ab&pid=1-s2.0-S0361923024001722-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141874213","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

BOC targets SMO to regulate the Hedgehog pathway and promote proliferation, migration, and invasion of glioma cells BOC 以 SMO 为靶点调控刺猬蛋白通路，促进胶质瘤细胞的增殖、迁移和侵袭

IF 3.5 3区医学

Brain Research Bulletin Pub Date : 2024-07-30 DOI: 10.1016/j.brainresbull.2024.111037

{"title":"BOC targets SMO to regulate the Hedgehog pathway and promote proliferation, migration, and invasion of glioma cells","authors":"","doi":"10.1016/j.brainresbull.2024.111037","DOIUrl":"10.1016/j.brainresbull.2024.111037","url":null,"abstract":"<div><p>The purpose of this study was to investigate the effects of BOC on glioblastoma cells and its underlying mechanisms. <em>In vitro</em>, BOC-knockdown was performed in glioma cell lines. CCK-8 and Transwell were used to assess the impact of BOC on the viability, invasion, and migration of gliobma cells. RNA-seq technology was employed to analyze the differential gene expression between BOC-knockdown glioma cells and the control group, and qRT-PCR was used to validate the expression of downstream differential genes. SMO-overexpression was performed to investigate the effects of SMO on glioma cells. A BOC-knockdown mouse subcutaneous tumor model was to verify the effects of BOC on mouse tumors. Tissue microarray technology was used to detect the expression of BOC and SMO in samples of normal human brain tissue and glioma tissue. <em>In vitro</em>, BOC-knockdown inhibited the viability, invasion, and migration of glioma cells, as well as downregulated the expression of downstream differential genes SMO, EGFR, HRAS, and MRAS. Conversely, SMO-overexpression upregulated the viability, invasion, and migration abilities of BOC-knockdown cells. <em>In vivo</em>, BOC-knockdown suppressed tumor growth in mice and downregulated the expression of downstream differential genes SMO, EGFR, HRAS, and MRAS. Tissue microarray results showed that both BOC and SMO were highly expressed in glioma tissues. BOC is aberrantly overexpressed in glioma patients and promotes glioma development. Mechanistically, BOC activates the Hedgehog (Hh) and RAS signaling pathways by upregulating the expression of SMO, EGFR, HRAS, and MRAS, thereby facilitating the Proliferation, invasion and migration of glioma cells.</p></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0361923024001709/pdfft?md5=672774fbe523a71496e2c0e98ab7363f&pid=1-s2.0-S0361923024001709-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141795851","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Electroacupuncture alleviates motor dysfunction by regulating neuromuscular junction disruption and neuronal degeneration in SOD1G93A mice 电针通过调节 SOD1G93A 小鼠神经肌肉接头紊乱和神经元退化缓解运动功能障碍

IF 3.5 3区医学

Brain Research Bulletin Pub Date : 2024-07-29 DOI: 10.1016/j.brainresbull.2024.111036

{"title":"Electroacupuncture alleviates motor dysfunction by regulating neuromuscular junction disruption and neuronal degeneration in SOD1G93A mice","authors":"","doi":"10.1016/j.brainresbull.2024.111036","DOIUrl":"10.1016/j.brainresbull.2024.111036","url":null,"abstract":"<div><p>Amyotrophic lateral sclerosis (ALS) is a fatal neurological disease characterized by the progressive destruction of the neuromuscular junction (NMJ) and the degeneration of motor neurons, eventually leading to atrophy and paralysis of voluntary muscles responsible for motion and breathing. NMJs, synaptic connections between motor neurons and skeletal muscle fibers, are extremely fragile in ALS. To determine the effects of early electroacupuncture (EA) intervention on nerve reinnervation and regeneration following injury, a model of sciatic nerve injury (SNI) was first established using SOD1<sup>G93A</sup> mice, and early electroacupuncture (EA) intervention was conducted at Baihui (DU20), and bilateral Zusanli (ST36). The results revealed that EA increased the Sciatic nerve Functional Index, the structural integrity of the gastrocnemius muscles, and the cross-sectional area of muscle fibers, as well as up-regulated the expression of acetylcholinesterase and facilitated the co-location of α7 nicotinic acetate choline receptors and α-actinin. Overall, these results suggested that EA can promote the repair and regeneration of injured nerves and delay NMJ degeneration in SOD1<sup>G93A</sup>-SNI mice. Moreover, analysis of the cerebral cortex demonstrated that EA alleviated cortical motor neuron damage in SOD1<sup>G93A</sup> mice, potentially attributed to the inhibition of the cyclic GMP-AMP synthase-stimulator of interferon genes pathway and the release of interferon-β suppressing the activation of natural killer cells and the secretion of interferon-γ, thereby further inhibiting microglial activation and the expression of inflammatory factors. In summary, EA delayed the degeneration of NMJ and mitigated the loss of cortical motor neurons, thus delaying disease onset, accompanied by alleviation of muscle atrophy and improvements in motor function in SOD1<sup>G93A</sup> mice.</p></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0361923024001692/pdfft?md5=edd40ca08602c566fac33a6611ea7f4a&pid=1-s2.0-S0361923024001692-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141859072","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Acupuncture, an effective treatment for post-stroke neurologic dysfunction 针灸是治疗中风后神经功能障碍的有效方法。

IF 3.5 3区医学

Brain Research Bulletin Pub Date : 2024-07-26 DOI: 10.1016/j.brainresbull.2024.111035

{"title":"Acupuncture, an effective treatment for post-stroke neurologic dysfunction","authors":"","doi":"10.1016/j.brainresbull.2024.111035","DOIUrl":"10.1016/j.brainresbull.2024.111035","url":null,"abstract":"<div><p>Stroke episodes represent a significant subset of cerebrovascular diseases globally, often resulting in diverse neurological impairments such as hemiparesis, spasticity, dysphagia, sensory dysfunction, cognitive impairment, depression, aphasia, and other sequelae. These dysfunctions markedly diminish patients' quality of life and impose substantial burdens on their families and society. Consequently, the restoration of neurological function post-stroke remains a primary objective of clinical treatment. Acupuncture, a traditional Chinese medicine technique, is endorsed by the World Health Organization (WHO) for stroke treatment due to its distinct advantages in managing cerebrovascular diseases, including ischemic stroke. Numerous clinical studies have substantiated the efficacy of acupuncture in ameliorating neurological dysfunctions following stroke. This review systematically examines the improvements in post-stroke neurological dysfunction attributable to acupuncture treatment and elucidates potential mechanisms of action proposed in recent years. Additionally, this article aims to present novel therapeutic concepts and strategies for the clinical management of post-stroke neurological dysfunction.</p></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0361923024001680/pdfft?md5=66f6ced528fdc4fd12e64df7d5abdb53&pid=1-s2.0-S0361923024001680-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141787346","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Intermittent fasting alleviates postoperative cognitive dysfunction by reducing neuroinflammation in aged mice 间歇性禁食可通过减少老年小鼠的神经炎症缓解术后认知功能障碍。

IF 3.5 3区医学

Brain Research Bulletin Pub Date : 2024-07-23 DOI: 10.1016/j.brainresbull.2024.111034

{"title":"Intermittent fasting alleviates postoperative cognitive dysfunction by reducing neuroinflammation in aged mice","authors":"","doi":"10.1016/j.brainresbull.2024.111034","DOIUrl":"10.1016/j.brainresbull.2024.111034","url":null,"abstract":"<div><p>Elderly individuals undergoing surgical procedures are often confronted with the peril of experiencing postoperative cognitive dysfunction (POCD). Prior research has demonstrated the exacerbating effect of sevoflurane anesthesia on neuroinflammation, which can further deteriorate the condition of POCD in elderly patients. Intermittent fasting (IF) restricts food consumption to a specific time window and has been demonstrated to ameliorate cognitive dysfunction induced by neuropathic inflammation. We subjected 18-month-old male mice to 16 hours of fasting and 8 hours of unrestricted eating over a 24-hour period for 0, 1, 2, and 4 weeks, followed by abdominal exploration under sevoflurane anesthesia. In this study, we aim to explore the potential impact of IF on postoperative cognitive function in aged mice undergoing sevoflurane surgery through the preoperative implementation of IF measures. The findings indicate two weeks of IF leads to a significant enhancement of learning and memory capabilities in mice following surgery. The cognitive performance, as determined by the novel object recognition and Morris water maze tests, as well as the synaptic plasticity, as measured by in vivo electrophysiological recordings, has demonstrated marked improvements. Furthermore, the administration of IF markedly enhances the expression of synaptic-associated proteins in hippocampal neurons, concomitant with a decreasing expression of pro-inflammatory factors and a reduced density of microglial cells within the hippocampal brain region. To summarize, the results of this study indicate that IF may mitigate inflammation in the hippocampal area of the brain. Furthermore, IF appears to provide a safeguard against cognitive impairment and synaptic plasticity impairment brought on by sevoflurane anesthesia.</p></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0361923024001679/pdfft?md5=98452d5ffd92ae7d19567434f1ccaf7f&pid=1-s2.0-S0361923024001679-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141757235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Up-regulation of BMAL1 by epigallocatechin-3-gallate improves neurological damage in SBI rats 表没食子儿茶素-3-棓酸盐上调 BMAL1 可改善 SBI 大鼠的神经损伤。

IF 3.5 3区医学

Brain Research Bulletin Pub Date : 2024-07-20 DOI: 10.1016/j.brainresbull.2024.111033

{"title":"Up-regulation of BMAL1 by epigallocatechin-3-gallate improves neurological damage in SBI rats","authors":"","doi":"10.1016/j.brainresbull.2024.111033","DOIUrl":"10.1016/j.brainresbull.2024.111033","url":null,"abstract":"<div><p>Brain Muscle ARNT-Like Protein 1 (BMAL1) suppresses oxidative stress in brain injury during surgery. Epigallocatechin-3-gallate (EGCG), a monomer in green tea, has been identified as an antioxidant and a potential agonist for BMAL1. In this work, the mechanism by which BMAL1 is regulated was investigated, as well as the therapeutic effect of EGCG on surgically injured rats. The pathological environment after brain injury during surgery was simulated by excising the right frontal lobe of rats. Rats received an intraperitoneal injection of EGCG immediately after surgery. Neurological scores and cerebral edema were recorded after surgery. Fluoro-Jade C staining, TUNEL staining, western blot, and lipid peroxidation analyses were conducted 3 days later. Here we show that the endogenous BMAL1 level decreased after brain injury. Postoperative administration of EGCG up-regulated the content of BMAL1 around the cerebral cortex, reduced the oxidative stress level, reduced neuronal apoptosis and the number of degenerated neurons, alleviated cerebral edema, and improved neurological scores in rats. This suggests that BMAL1 is an effective target for treating surgical brain injury, as well as that EGCG may be a promising agent for alleviating postoperative brain injury.</p></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0361923024001667/pdfft?md5=63d9e62716f1cf79f92e1a8b59b34006&pid=1-s2.0-S0361923024001667-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141733637","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Buyang Huanwu Decoction suppresses ischemic stroke by suppressing glycolysis and cell apoptosis in rat brain microvascular endothelial cells 步阳黄酒汤通过抑制大鼠脑微血管内皮细胞的糖酵解和细胞凋亡，抑制缺血性中风的发生

IF 3.5 3区医学

Brain Research Bulletin Pub Date : 2024-07-17 DOI: 10.1016/j.brainresbull.2024.111032

{"title":"Buyang Huanwu Decoction suppresses ischemic stroke by suppressing glycolysis and cell apoptosis in rat brain microvascular endothelial cells","authors":"","doi":"10.1016/j.brainresbull.2024.111032","DOIUrl":"10.1016/j.brainresbull.2024.111032","url":null,"abstract":"<div><h3>Background</h3><p>Buyang Huanwu Decoction (BHD) is widely used in Chinese clinical practice for the treatment and prevention of ischemic cerebral vascular diseases. This study was designed to investigate the effects of BHD on ischemic stroke (IS) and its underlying mechanism.</p></div><div><h3>Methods</h3><p>The middle cerebral artery occlusion (MCAO) rat model and oxygen-glucose deprivation and reoxygenation (OGD/R) rat brain microvascular endothelial cell (RBMVEC) models were established. Brain infarction size and neurological score were calculated following MCAO surgery. Evans blue was used to measure blood brain barrier (BBB) permeability. Cell counting kit-8 (CCK-8) and TUNEL assays were performed to evaluate the cell viability and apoptosis of RBMVECs. Dual-luciferase reporter assay was used to analyze the transcriptional activities of apoptosis-related genes.</p></div><div><h3>Results</h3><p>Results showed that higher infarction volume, neurological scores, and BBB permeability in the MCAO group rats were reduced after BHD treatment. Drug serum (DS) treatment had no impact on the normal RBMVECs’ cell viability and cell apoptosis. Besides, DS treatment decreased the lactate production, glucose uptake, and extracellular acidification rate in normal and OGD/R-induced RBMVECs. DS treatment downregulated the protein levels of pan-lysine lactylation (kla), histone H3 lysine 18 lactylation (H3K18la), and the transcriptional of apoptotic protease activating factor-1 (Apaf-1) in OGD/R-treated RBMVECs. In addition, Apaf-1 overexpression decreased cell viability and increased apoptosis and glycolysis activity of OGD/R-treated RBMVECs.</p></div><div><h3>Conclusion</h3><p>In summary, BHD inhibited glycolysis and apoptosis via suppressing the pan-kla and H3K18la protein levels and the Apaf-1 transcriptional activity, thus restraining the progression of IS.</p></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0361923024001655/pdfft?md5=5f1e15fe27b32d0300267c692f4caedb&pid=1-s2.0-S0361923024001655-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141639998","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0