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Neuronal nitric oxide synthase/reactive oxygen species pathway is involved in apoptosis and pyroptosis in Epilepsy

Neural Regeneration Research 2023年第6期18卷 1277-1285页

作者： Xiao-Xue Xu Rui-Xue Shi Yu Fu Jia-Lu Wang Xin Tong Shi-Qi Zhang Na Wang Mei-Xuan Li Yu Tong Wei Wang Miao He Bing-Yang Liu Gui-Lan Chen Feng Guo Department of Pharmaceutical Toxicology School of Pharmaceutical ScienceChina Medical UniversityShenyangLiaoning ProvinceChina Department of Neurology the First Affiliated Hospital of China Medical UniversityShenyangLiaoning ProvinceChina Key Laboratory of Medical Electrophysiology Ministry of Education&Medical Electrophysiological Key Laboratory of Sichuan ProvinceInstitute of Cardiovascular ResearchSouthwest Medical UniversityLuzhouSichuan ProvinceChina Department of Endocrinology and Metabolism the Fourth Affiliated Hospital of China Medical UniversityShenyangLiaoning ProvinceChina Department of Endocrinology Shengjing Hospital of China Medical UniversityShenyangLiaoning ProvinceChina

Dysfunction of neuronal nitric oxide synthase contributes to neurotoxicity,which triggers cell death in various neuropathological diseases,including Epilepsy.Studies have shown that inhibition of neuronal nitric oxide synthase activity increases the Epilepsy threshold,that is,has an anticonvulsant effect.However,the exact role and potential mechanism of neuronal nitric oxide synthase in seizures are still unclear.In this study,we performed RNA sequencing,functional enrichment analysis,and weighted gene coexpression network analysis of the hippocampus of tremor rats,a rat model of genetic Epilepsy.We found damaged hippocampal mitochondria and abnormal succinate dehydrogenase level and Na+-K+-ATPase activity.In addition,we used a pilocarpine-induced N2a cell model to mimic epileptic injury.After application of neuronal nitric oxide synthase inhibitor 7-nitroindazole,changes in malondialdehyde,lactate dehydrogenase and superoxide dismutase,which are associated with oxidative stress,were reversed,and the increase in reactive oxygen species level was reversed by 7-nitroindazole or reactive oxygen species inhibitor N-acetylcysteine.Application of 7-nitroindazole or N-acetylcysteine downregulated the expression of caspase-3 and cytochrome c and reversed the apoptosis of epileptic cells.Furthermore,7-nitroindazole or N-acetylcysteine downregulated the abnormally high expression of NLRP3,gasdermin-D,interleukin-1βand interleukin-18.This indicated that 7-nitroindazole and N-acetylcysteine each reversed epileptic cell death.Taken together,our findings suggest that the neuronal nitric oxide synthase/reactive oxygen species pathway is involved in pyroptosis of epileptic cells,and inhibiting neuronal nitric oxide synthase activity or its induced oxidative stress may play a neuroprotective role in Epilepsy.

关键词： apoptosis bioinformatics analysis cell death Epilepsy nitric oxide synthase oxidative stress pyroptosis RNA sequencing Tremor rat weighted gene co-expression network analysis

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Genotypic and phenotypic spectra of NBEA-related neurodevelopmental disorder with Epilepsy:a case series and literature review

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World Journal of Pediatrics 2022年第9期18卷 636-641页

作者： Zou Pan Chen Chen Fei Yin Jing Peng Department of Pediatrics Xiangya Hospital of Central South UniversityChangsha410008China Clinical Research Center for Children Neurodevelopmental Disabilities of Hunan Province Xiangya HospitalCentral South UniversityChangsha410008China

NBEA(MIM#604,889)is a novel disease causative gene that responds for neurodevelopment disorder with or without generalized Epilepsy(NEDEGE,MIM#619,157).It encodes neurobeachin protein,a multi-domain neuro-specific scaf-folding protein that plays a vital role in vesicle trafficking and synaptic structure.NBEA was initially observed in an idiopathic autism patient,and thus NBEA has been regarded as a candidate autism gene for nearly two decades[1-4].In 2018,Mulhern et al.reported 24 individuals with de novo heterozygous NBEA variants with neurodevelopmental delay with autism and early onset generalized Epilepsy,which led the Online Mendian Inheritance in Man(OMIM)team to identify it as a disease-causing gene for NEDEGE[5].Since then,only a few NBEA-related cases with similar clinical phenotypes have been reported[6-8].

关键词： Epilepsy structure.

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Burden of Epilepsy in China and its provinces,1990 to 2019:findings from the Global Burden of Disease Study 2019

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Chinese Medical Journal 2023年第3期136卷 305-312页

作者： Wei Liu Yangyang Xu Yicong Lin Lijun Wang Maigeng Zhou Peng Yin Guoguang Zhao National Center for Chronic and Non-Communicable Disease Control and Prevention Chinese Center for Disease Control and PreventionBeijing 100050China Department of Neurology Xuanwu HospitalCapital Medical UniversityNational Center for Neurological DisordersBeijing 100053China Department of Neurosurgery Xuanwu HospitalCapital Medical UniversityNational Center for Neurological DisordersBeijing 100053China

Background: Epilepsy accounts for a significant portion of the global disease burden. However, little is known about the disease burden of Epilepsy in China and its provinces. Methods: We assessed the burden of Epilepsy in China and its provinces, municipalities, and autonomous regions from 1990 to 2019. Burden was measured as incidence, prevalence, deaths, years lived with disability, years of life lost, and disability-adjusted life years (DALYs), by age, sex, year, and province. We used the Socio-Demographic Index (SDI) to determine the association between the provincial development level and age-standardized DALY rates of Epilepsy from 1990 to 2019. Results: In 2019, Epilepsy caused 1367.51 thousand (95% uncertainty interval [UI]: 979.92–1837.61 thousand) DALYs, and the age-standardized DALY rate was 99.77 (95% UI: 71.33–133.52)/100,000. The age-standardized incidence and prevalence rates for Epilepsy in China were 24.65/100,000 and 219.69/100,000, increased by 45.00% (95% UI: 8.03–98.74%) and 35.72% (95% UI: 0.47–86.19%) compared with that in 1990, respectively. From 1990 to 2019, the proportion of DALY caused by Epilepsy in the age group under 25 years steadily decreased. The proportion of DALYs caused by Epilepsy in people aged 50 years and over increased from 9.45% and 10.22% in 1990 to 29.01% and 32.72% for male and female individuals in 2019, respectively. The highest age-standardized mortality rates were seen in Tibet (4.26 [95% UI: 1.43–5.66]/100,000), Qinghai (1.80 [95% UI: 1.15–2.36]/100,000), and Yunnan (1.30 [95% UI: 0.88–1.62]/100,000), and the lowest mortality rates were in Guangdong (0.48 [95% UI: 0.39–0.64]/100,000), Zhejiang (0.56 [95% UI: 0.44–0.70]/100,000), and Shanghai (0.57 [95% UI: 0.41–0.73]/100,000). The age-standardized DALY rates across the country and in provinces, municipalities, and autonomous regions generally decreased as their SDI increased. Conclusions: The disease burden of Epilepsy is still heavy in China, especially in the western provinces. The incidence and prevalence of

关键词： Aged Epilepsy Global Burden of disease Quality-adjusted life years Disability-adjusted life years Incidence Prevalence China

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MicroRNAs in mouse and rat models of experimental Epilepsy and potential therapeutic targets

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Neural Regeneration Research 2023年第10期18卷 2108-2118页

作者： Bridget Martinez Philip V.Peplow Department of Pharmacology University of Nevada-RenoRenoNVUSA Department of Medicine University of Nevada-RenoRenoNVUSA Department of Anatomy University of OtagoDunedinNew Zealand

Epilepsy is a common and serious neurological disease that causes recurrent seizures. The brain damage caused by seizures can lead to depression, anxiety, cognitive impairment, or disability. In almost all cases chronic seizures are difficult to cure. MicroRNAs are widely expressed in the central nervous system and play important roles in the pathogenesis of several neurological disorders, including Epilepsy. A variety of animals(mostly mice and rats) have been used to induce experimental Epilepsy using different protocols and miRNA profiling performed. Most of the recent studies reviewed had performed miRNA profiling in hippocampal tissues and a large number of microRNAs were dysregulated when compared to controls. Most notably, miR-132-3p,-146a-5p,-10a-5p,-21a-3p,-27a-3p,-142a-5p,-212-3p,-431-5p, and-155 were upregulated in both the mouse and rat studies. Overexpression of miR-137 and miR-219 decreased seizure severity in a mouse epileptic model, and suppression of miR-451,-10a-5p,-21a-5p,-27a-5p,-142a-5p,-431-5p,-155, and-134 had a positive influence on seizure behavior. In the rat studies, overexpression of miR-139-5p decreased neuronal damage in drug-resistant rats and inhibition of miR-129-2-3p,-27a-3p,-155,-134,-181a, and-146a had a positive effect on seizure behavior and/or reduced the loss of neuronal cells. Further studies are warranted using adult female and immature male and female animals. It would also be helpful to test the ability of specific agomirs and antagomirs to control seizure activity in a subhuman primate model of Epilepsy such as adult marmosets injected intraperitoneally with pilocarpine or cynomolgus monkeys given intrahippocampal injections of kainic acid.

关键词： Epilepsy experimental models microRNA mouse rat seizures therapeutic targets

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CXCR5 Regulates Neuronal Polarity Development and Migration in the Embryonic Stage via F‑Actin Homeostasis and Results in Epilepsy‑Related Behavior

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Neuroscience Bulletin 2023年第11期39卷 1605-1622页

作者： Zhijuan Zhang Hui Zhang Ana Antonic‑Baker Patrick Kwan Yin Yan Yuanlin Ma Department of Neurology Chongqing Key Laboratory of NeurologyThe First Affiliated Hospital of Chongqing Medical UniversityChongqing 400016China Chongqing Emergency Medical Center The First Affiliated Hospital of Chongqing Medical UniversityChongqing 400016China Department of Neuroscience Central Clinical SchoolMonash UniversityMelbourneAustralia

Epilepsy is a common,chronic neurological disorder that has been associated with impaired neurodevelopment and immunity.The chemokine receptor CXCR5 is involved in seizures via an unknown mechanism.Here,we first determined the expression pattern and distribution of the CXCR5 gene in the mouse brain during different stages of development and the brain tissue of patients with Epilepsy.Subsequently,we found that the knockdown of CXCR5 increased the susceptibility of mice to pentylenetetrazol-and kainic acid-induced seizures,whereas CXCR5 overexpression had the opposite effect.CXCR5 knockdown in mouse embryos via viral vector electrotransfer negatively influenced the motility and multipolar-to-bipolar transition of migratory neurons.Using a human-derived induced an in vitro multipotential stem cell neurodevelopmental model,we determined that CXCR5 regulates neuronal migration and polarization by stabilizing the actin cytoskeleton during various stages of neurodevelopment.Electrophysiological experiments demonstrated that the knockdown of CXCR5 induced neuronal hyperexcitability,resulting in an increased number of seizures.Finally,our results suggested that CXCR5 deficiency triggers seizure-related electrical activity through a previously unknown mechanism,namely,the disruption of neuronal polarity.

关键词： Epilepsy CXCR5 Embryonic neurogenesis Pluripotent stem cells Intrauterine electroporation F-actin Neuronal polarity Neuronal migration

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Double-Edged Mossy Cells in Temporal Lobe Epilepsy:Evil in the Early Stage Through a BDNF-Dependent Strengthening Dentate Gyrus Circuit

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Neuroscience Bulletin 2023年第6期39卷 1031-1033页

作者： Heming Cheng Qiuwen Lou Yi Wang Zhong Chen Key Laboratory of Neuropharmacology and Translational Medicine of Zhejiang Province School of Pharmaceutical SciencesZhejiang Chinese Medical UniversityHangzhou310053China Department of Neurology The Third Affiliated Hospital of Zhejiang Chinese Medical UniversityHangzhou310053China Institute of Pharmacology and Toxicology College of Pharmaceutical SciencesZhejiang UniversityHangzhou310058China

Temporal lobe Epilepsy(TLE),one of the most common drug-resistant epilepsies,is characterized by abnormal recurrent excitatory activity originating from the temporal lobe.In the dentate gyrus(DG)of the hippocampus.

关键词： Epilepsy Moss Temporal

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Revealing the Precise Role of Calretinin Neurons in Epilepsy: We Are on the Way

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Neuroscience Bulletin 2022年第2期38卷 209-222页

作者： Yingbei Qi Heming Cheng Yi Wang Zhong Chen Institute of Pharmacology and Toxicology College of Pharmaceutical SciencesZhejiang UniversityHangzhouChina Key Laboratory of Neuropharmacology and Translational Medicine of Zhejiang Province School of Pharmaceutical SciencesZhejiang Chinese Medical UniversityHangzhouChina

Epilepsy is a common neurological disorder characterized by hyperexcitability in the brain.Its pathogenesis is classically associated with an imbalance of excitatory and inhibitory neurons.Calretinin(CR)is one of the three major types of calcium-binding proteins present in inhibitory GABAergic neurons.The functions of CR and its role in neural excitability are still unknown.Recent data suggest that CR neurons have diverse neurotransmitters,morphologies,distributions,and functions in different brain regions across various species.Notably,CR neurons in the hippocampus,amygdala,neocortex,and thalamus are extremely susceptible to excitotoxicity in the epileptic brain,but the causal relationship is unknown.In this review,we focus on the heterogeneous functions of CR neurons in different brain regions and their relationship with neural excitability and Epilepsy.Importantly,we provide perspectives on future investigations of the role of CR neurons in Epilepsy.

关键词： Calretinin Epilepsy Calcium-binding protein Neuronal excitability

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Anti-Seizure and Neuronal Protective Effects of Irisin in Kainic Acid-Induced Chronic Epilepsy Model with Spontaneous Seizures

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Neuroscience Bulletin 2022年第11期38卷 1347-1364页

作者： Jie Yu Yao Cheng Yaru Cui Yujie Zhai Wenshen Zhang Mengdi Zhang Wenyu Xin Jia Liang Xiaohong Pan Qiaoyun Wang Hongliu Sun School of Pharmaceutical Sciences Binzhou Medical UniversityYantai 264003China The Sixth Scientifc Research Department Shandong Institute of Nonmetallic MaterialsJinan 250031China

An increased level of reactive oxygen species is a key factor in neuronal apoptosis and epileptic seizures.Irisin reportedly attenuates the apoptosis and injury induced by oxidative stress.Therefore,we evaluated the effects of exogenous irisin in a kainic acid(KA)-induced chronic spontaneous Epilepsy rat model.The results indicated that exogenous irisin significantly attenuated the KA-induced neuronal injury,learning and memory defects,and seizures.Irisin treatment also increased the levels of brain-derived neurotrophic factor(BDNF)and uncoupling protein 2(UCP2),which were initially reduced following KA administration.Furthermore,the specific inhibitor of UCP2(genipin)was administered to evaluate the possible protective mechanism of irisin.The reduced apoptosis,neurodegeneration,and spontaneous seizures in rats treated with irisin were significantly reversed by genipin administration.Our findings indicated that neuronal injury in KA-induced chronic Epilepsy might be related to reduced levels of BDNF and UCP2.Moreover,our results confirmed the inhibition of neuronal injury and epileptic seizures by exogenous irisin.The protective effects of irisin may be mediated through the BDNF-mediated UCP2 level.Our results thus highlight irisin as a valuable therapeutic strategy against neuronal injury and epileptic seizures.

关键词： Epilepsy Seizure Irisin Genipin Neuronal injury

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Effects of intensive psychological intervention on treatment compliance,psychological status,and quality of life of patients with Epilepsy

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World Journal of Psychiatry 2024年第5期14卷 670-677页

作者： Su-Hua Zhang Jie-Hua Wang Hong-Yu Liu Yue-Xia Zhang Ya-Ling Lin Bi-Yu Wu Department of Neurology Quanzhou First HospitalQuanzhou 362000Fujian ProvinceChina Department of Nursing Quanzhou First HospitalQuanzhou 362000Fujian ProvinceChina

BACKGROUND Epilepsy is a nervous system disease characterized by recurrent attacks,a long disease course,and an unfavorable prognosis.It is associated with an enduring therapeutic process,and finding a cure has been difficult.Patients with Epilepsy are predisposed to adverse moods,such as resistance,anxiety,nervousness,and anxiety,which compromise treatment compliance and overall efficacy.AIM To explored the influence of intensive psychological intervention on treatment compliance,psychological status,and quality of life(QOL)of patients with Epilepsy.METHODS The clinical data of 105 patients with Epilepsy admitted between December 2019 and July 2023 were retrospectively analyzed,including those of 50 patients who underwent routine intervention(control group)and 55 who underwent intensive psychological intervention(research group).Treatment compliance,psychological status based on the Self-Rating Anxiety Scale(SAS)and Depression Scale Self-Rating Depression Scale(SDS)scores,hope level assessed using the Herth Hope Scale(HHS),psychological resilience evaluated using the Psychological Resilience Scale,and QOL determined using the QOL in Epilepsy-31 Inventory(QOLIE-31)were comparatively analyzed.RESULTS Treatment compliance in the research group was 85.5%,which is significantly better than the 68.0%of the control group.No notable intergroup differences in preinterventional SAS and SDS scores were identified(P>0.05);however,after the intervention,the SAS and SDS scores decreased significantly in the two groups,especially in the research group(P0.05).After 6 months of intervention,the research group showed evidently higher HHS,CD-RISC,tenacity,optimism,strength,and QOLIE-31 scores(PEpilepsy.

关键词： Intensive psychological intervention Epilepsy Treatment compliance Psychological status Quality of life

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Current role of surgery for tuberous sclerosis complex-associated Epilepsy

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Pediatric Investigation 2022年第1期6卷 16-22页

作者： Nicola Specchio Giusy Carfi Pavia Luca de Palma Alessandro De Benedictis Chiara Pepi Marta Conti Carlo Efisio Marras Federico Vigevano Paolo Curatolo Rare and Complex Epilepsy Unit Department of NeurosciencesBambino GesùChildren’s HospitalIRCCSRomeItaly Neurosurgery Unit Department of NeurosciencesBambino GesùChildren’s HospitalIRCCSRomeItaly Department of Neurosciences Bambino GesùChildren’s HospitalIRCCSRomeItaly Child Neurology and Psychiatry Unit Systems Medicine DepartmentTor Vergata UniversityRomeItaly

Tuberous sclerosis complex(TSC)is a rare multisystem,autosomal dominant neurocutaneous syndrome in which Epilepsy is the most common of several neurological and psychiatric manifestations.Around two thirds of patients develop drug-resistant Epilepsy for whom surgical resection of epileptogenic foci is indicated when seizures remain inadequately controlled following trial of two antiseizure medications.The challenge with presurgical and surgical approaches with patients with TSC is overcoming the complexity from the number of tubers and the multiplex epileptogenic network forming the epileptogenic zone.Data suggest that seizure freedom is achieved by 55%-60%of patients,but predictive factors for success have remained elusive,which makes for unconfident selection of surgical candidates.This article presents three different cases as illustrations of the potential challenges faced when assessing the suitability of TSC patients for Epilepsy surgery.

关键词： Epilepsy Everolimus Imaging Prognostics Surgery Tuberous sclerosis complex(TSC)

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