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neuronal injury and brain-derived neurotrophic factor expression in a rat model of amygdala kindling seizures Differences in brain regions and kindling courses

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Neural Regeneration Research 2010年第8期5卷 585-590页

作者： Weihong Lin Hongmei Meng Yudan Lv Zan Wang Na Li Li Cui Baimin Zhang Department of Neurology First Hospital of Jilin UniversityChangchun 130021Jilin ProvinceChina

BACKGROUND：Studies have demonstrated that brain-derived neurotrophic factor （BDNF） has a dual effect on epilepsy. However, the relationship between epilepsy-induced brain injury and BDNF remains poorly ***：According to ultrastructural and molecular parameters, to detect the degree of neuronal injury and BDNF expression changes at different brain regions and different kindling times to determine the effects of BDNF on epilepsy-induced brain ***, TIME AND SETTING：A randomized, controlled, animal experiment based on neuropathology and molecular biology was performed at the Department of Physiology and Department of Pathology, Basic Medical College of Jilin University in ***：UltraSensitiveTM SP kit for immunohistochemistry （Fuzhou Maxim Biotechnology, China）, BDNF antibody （concentrated type, Wuhan Boster Biological Technology, China）, JEM-1000SX transmission electron microscopy （JEOL, Japan）, and BH-2 light microscope （Olympus, Japan） were used in the present ***：Wistar rats were randomly assigned to control （n = 6）, sham-surgery （n = 6）, and model （n = 60） groups. The control group rats were not treated; an electrode was embedded into the amygdala in rats from the sham-surgery and model groups; an amygdala kindling epilepsy model was established in the model *** OUTCOME MEASURES：Pathological changes in the temporal lobe and hippocampus were observed by light and electron microscopy at 1, 3, 7, 14, and 21 days following kindling, and BDNF expression in the various brain regions was determined by ***：In the model group, temporal lobe cortical and hippocampal neurons were swollen and the nuclei were laterally deviated. There were also some apoptotic neurons 3 days after kindling. The nucleoli disappeared and the nuclei appeared broken or lysed, as well as slight microglia hyperplasia, at 7 days. Electron microscopic observation displayed chromatin aggregation in the nuclei and slight mitochon

关键词： epilepsy brain injury brain-derived neurotrophic factor kindling brain regions rats neuronal injury neural regeneration

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Cysteinyl leukotriene receptors CysLT1 and CysLT2 are upregulated in acute neuronal injury after focal cerebral ischemia in mice

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Acta Pharmacologica Sinica 2006年第12期27卷 1553-1560页

作者： Yan-jun ZHANG~(2,3)Lei ZHANG~2 Yi-lu YE~2 San-hua FANG~2 Yu ZHOU~2 Wei-ping ZHANG~2 Yun-bi LU~2 Er-qing WEI~(2,4)2 Department of Pharmacology,School of Medicine,Zhejiang University,Hangzhou 310058 3 Zhejiang Provincial Centre for Disease Control and Prevention,Hangzhou 310009,China DepartmentofPharmacology SchoolofMedicineZhejiangUniversityHangzhou310058 ZhejiangProvincialCentreforDiseaseControlandPrevention Hangzhou310009China

Aim:To determine whether cysteinyl leukotriene receptors（CysLT1and CysLT2）are upregulated in acute neuronal injury after focal cerebral ischemia in mice,andto confirm CysLT1receptor ***:After permanent focal cerebralischemia was induced by middle cerebral artery occlusion（MCAO）,neurologicaldeficits and neuron loss were determined at various time points within *** expressions of CysLT1and CysLT2receptors in the brain were analyzed ***1receptor localization was detected by double ***:Neurological deficits and neuron loss were found 6,24 and 48h *** mRNA expressions of both CysLT1and CysLT2receptors wereupregulated in the ischemic hemisphere 1,24,and 48 h after MCAO with peaks at24 *** CysLT1receptor was selectively localized in neurons 24 h after ***:CysLT1and CysLT2receptors are upregulated in acute neuronal in-jury after focal cerebral ischemia,and the CysLT1receptor is localized in neuronsafter ischemia.

关键词： cysteinyl leukotriene receptor cerebral ischemia neuronal injury mRNA expression

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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 *** reportedly attenuates the apoptosis and injury induced by oxidative ***,we evaluated the effects of exogenous irisin in a kainic acid(KA)-induced chronic spontaneous epilepsy rat *** results indicated that exogenous irisin significantly attenuated the KA-induced neuronal injury,learning and memory defects,and *** treatment also increased the levels of brain-derived neurotrophic factor(BDNF)and uncoupling protein 2(UCP2),which were initially reduced following KA ***,the specific inhibitor of UCP2(genipin)was administered to evaluate the possible protective mechanism of *** reduced apoptosis,neurodegeneration,and spontaneous seizures in rats treated with irisin were significantly reversed by genipin *** findings indicated that neuronal injury in KA-induced chronic epilepsy might be related to reduced levels of BDNF and ***,our results confirmed the inhibition of neuronal injury and epileptic seizures by exogenous *** protective effects of irisin may be mediated through the BDNF-mediated UCP2 *** 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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Ocimum sanctum extract preserves neuronal echotexture and controls seizure in lithium-pilocarpine induced status epilepticus rats

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Asian Pacific Journal of Tropical Biomedicine 2023年第11期13卷 479-487,I0009页

作者： Soumya Sucharita Pattnaik Sudhir Chandra Sarangi Deeksha Sharma Surabhi Sinha Tapas C Nag Aruna Nambirajan Manjari Tripathi Department of Pharmacology All India Institute of Medical SciencesNew DelhiIndia Department of Anatomy All India Institute of Medical SciencesNew DelhiIndia Department of Pathology All India Institute of Medical SciencesNew DelhiIndia Department of Neurology All India Institute of Medical SciencesNew DelhiIndia

Objective:To investigate the effect of Ocimum sanctum hydroalcoholic extract(OSHE)on seizure control and neuronal injury in rats with lithium-pilocarpine-induced status epilepticus(SE).Methods:SE was induced by administering lithium chloride followed by pilocarpine 24 h *** was administered either alone or in combination with valproate(VPA)3 days before SE induction until 14 days post-SE *** parameters were recorded on day 1(0-3 h),day 1-3 and day 4-14 *** day 14 post-SE,neurobehavioural tests(elevated plus maze and passive avoidance)were done followed by total antioxidant capacity,neuron-specific enolase,immunohistochemistry,and electron microscopic assessment in the hippocampus and cortex ***:OSHE+VPA provided more significant seizure protection(75%)than VPA(62.5%),OSHE(62.5%),or SE control(12.5%)(overall P=0.003).The latency to stage-3/4 seizures was increased and the number of stage-3/4 seizures was reduced in all treatment groups compared to the SE control group(P=0.002 andneuronal loss compared to the SE control in the hippocampus(Pneuronal echotexture and reducing oxidative stress in the hippocampus.

关键词： Status epilepticus Ocimum sanctum Seizure protection neuronal injury Electron microscopy

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neuronal PPARαdeficiency-induced axonal mitochondrial transport defects underly isch⁃emic stroke pathology

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中国药理学与毒理学杂志 2021年第9期35卷 681-682页

作者： XU Lan-xi ZHUO Ren-gong JIN Xin YANG Li-chao School of Medicine Xiamen UniversityXiamen 361005China

OBJECTIVE Peroxisome proliferator activated receptor alpha(PPARα)is an important protective factor in neurovascular diseases such as ischemic *** PPARαexpression is higher in neurons than astrocytes and microglia,the pathophysiological functions of neuronal specific-PPARαin isch⁃emic stroke remains ***,we report that neuronal PPARαdeficiency is a key factor of neuronal ***αexpression markedly decreased in neurons after ischemic *** AND RESULTS neuronal-specific PPARαknockout(NCKO)exacerbates neuronal damage and brain ischemic ***αdefi⁃ciency disrupts axonal microtubule organization and mitochondrial transport by decreasing the expression of dynein light chain Tctex-type 1(Dynlt1),which is implicated in cytoprotective role with damaged ***,resto⁃ration of Dynlt1 expression in neurons of NCKO mice rescue mitochondrial transport disorder,cognitive deficits and brain ischemic injury asso⁃ciated with PPARα*** These results reveal a critical role for neuronal PPARαin ischemic brain injury by modulating axonal mitochondrial transportation.

关键词： peroxisome proliferator activated receptor alpha mitochondrial dysfunction axonal transport neuronal injury ischemic stroke

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Treatment of radiation-induced brain injury with bisdemethoxycurcumin

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Neural Regeneration Research 2023年第2期18卷 416-421页

作者： Yun-Qian Chang Gui-Juan Zhou Hong-Mei Wen Duan-Qun He Chen-Lin Xu Ya-Rui Chen Yi-Hui Li Shuang-Xi Chen Zi-Jian Xiao Ming Xie Department of Neurology The First Affiliated HospitalHengyang Medical SchoolUniversity of South ChinaHengyangHunan ProvinceChina Department of Neurology The Second Affiliated HospitalHengyang Medical SchoolUniversity of South ChinaHengyangHunan ProvinceChina Department of Nursing Youxian People’s HospitalZhuzhouHunan ProvinceChina Department of Neurology Shenzhen Baoan People’s Hospital(Group)The Second People’s HospitalShenzhenGuangdong ProvinceChina Department of Neurology Xiangxi Autonomous Prefecture People’s HospitalJishouHunan ProvinceChina

Radiation therapy is considered the most effective non-surgical treatment for brain ***,there are no available treatments for radiation-induced brain ***(BDMC)is a demethoxy derivative of curcumin that has anti-proliferative,anti-inflammatory,and anti-oxidant *** determine whether BDMC has the potential to treat radiation-induced brain injury,in this study,we established a rat model of radiation-induced brain injury by administe ring a single 30-Gy vertical dose of irradiation to the whole brain,followed by intraperitoneal injection of 500μL of a 100 mg/kg BDMC solution every day for 5 successive *** res ults showed that BDMC increased the body weight of rats with radiation-induced brain injury,improved lea rning and memory,attenuated brain edema,inhibited astrocyte activation,and reduced oxidative *** findings suggest that BDMC protects against radiationinduced brain injury.

关键词： astrocytes bisdemethoxycurcumin brain edema brain tumor curcumin learning and memory neuronal injury oxidative stress radiation therapy radiation-induced brain injury

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Icariin Ameliorates D-galactose-induced Cell injury in Neuron-like PC12 Cells by Inhibiting MPTP Opening

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Current Medical Science 2024年第4期44卷 748-758页

作者： Shan-shan HU Tong-yao WANG Lu NI Fan-xin HU Bo-wen YUE Ying ZHENG Tian-lun WANG Abhishek KUMAR Yan-yan WANG Jin-e WANG Zhi-yong ZHOU Third-grade Pharmacological Laboratory of Traditional Chinese Medicine State Administration of Traditional Chinese MedicineChina Three Gorges UniversityYichang 443002China College of Medicine and Health Sciences China Three Gorges UniversityYichang 443002China College of Basic Medical Science China Three Gorges UniversityYichang 443002China

Objective Icariin(ICA)has a good neuroprotective effect and can upregulate neuronal basal autophagy in naturally aging *** dysfunction is associated with brain aging-related neurodegenerative *** opening of the mitochondrial permeability transition pore(mPTP)is a crucial factor in mitochondrial dysfunction and is associated with excessive *** study aimed to explore that ICA protects against neuronal injury by blocking the mPTP opening and down-regulating autophagy levels in a D-galactose(D-gal)-induced cell injury *** A cell model of neuronal injury was established in rat pheochromocytoma cells(PC12 cells)treated with 200 mmol/L D-gal for 48 *** this cell model,PC12 cells were pre-treated with different concentrations of ICA for 24 *** was used to detect cell *** associatedβ-galactosidase(SA-β-Gal)staining was used to observe cell *** blot analysis was performed to detect the expression levels of a senescence-related protein(p21),autophagy markers(LC3B,p62,Atg7,Atg5 and Beclin 1),mitochondrial fission and fusion-related proteins(Drp1,Mfn2 and Opa1),and mitophagy markers(Pink1 and Parkin).The changes of autophagic flow were detected by using mRFP-GFP-LC3 *** intracellular ultrastructure was observed by transmission electron *** was used to detect mPTP,mitochondrial membrane potential(MMP),mitochondrial reactive oxygen species(mtROS)and ROS *** and apoptosis levels were detected by flow *** D-gal treatment significantly decreased the viability of PC12 cells,and markedly increased the SA-β-Gal positive cells as compared to the control *** the D-gal stimulation,the expression of p21 was significantly ***,D-gal stimulation resulted in an elevated LC3B II/I ratio and decreased p62 ***,autophagosomes and autolysosomes were significantly increased,indicating abnormal activation of autophag

关键词： icariin neuronal injury mitochondrial dysfunction mitochondrial permeability transition pore autophagy

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Expression of inducible nitric oxide synthase in the brain tissue of rats at preoxygenation, hypoxia/reoxygenation

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Neural Regeneration Research 2006年第8期1卷 689-692页

作者： Hongzhi Chen Lu Li Hong Zhao Department of Anesthesiology Shengjing Hospital China Medical University Shenyang 110004 Liaoning ProvinceChina Department of AnesthesiologyShengjing Hospital China Medical University Shenyang 110004 Liaoning ProvinceChina Department of AnesthesiologyShengjing Hospital China Medical University Shenyang 110004 Liaoning ProvinceChina

BACKGROUND: The disorder of the respiratory and circulation system during the anesthesia and operation often can lead to severe hypoxia. Preoxygenation is a conventional therapy for treatment of hypoxia. OBJECTIVE: To observe the change in the expression of inducible nitric oxide synthase(iNOS), i.e. brain tissue injury degree, in cerebral cortex of rats after hypoxia/reoxygenation under the condition of different levels of preoxygenation. DESIGN: Randomized controlled animal experiment. SETTING: Department of Anesthesiology and Central Laboratory, Shengjing Hospital Affiliated to China Medical University. MATERIALS: This experiment was carried out in the laboratory of Shengjing Hospital Affiliated to China Medical University from March 2003 to March 2004. Seventy-two male Wistar rats, weighing from 250 to 300 g, were provided by the Animal Experimental Room of Shengjing Hospital of China Medical University [License No. SYXK (Liao) 2003-0019]. Seventy-two rats were randomized into 3 groups: preoxygenation group, hypoxia group and reoxygentation group. Each group was divided into 4 subgroups, 6 rats in each subgroup. METHODS: 0.21, 0.50, 0.75 and 0.98 volume fraction of oxygen was given to 4 subgroups of preoxygenation group respectively. The rats in each subgroup of hypoxia group inhaled oxygen for 30 minutes according to the method of preoxygenation. Then, nitrogen gas replaced oxygen and was pumped into the cabin, and the volume fraction of oxygen was decreased to be 0.05 within 20 minutes. The rats in each subgroup of reoxygenation group were treated with the experimental methods of preoxygenation and hypoxia separately, then they were moved into the wide mouthed bottle with two-air-duct rubber stopper. Finally, oxygen was pumped and the volume fraction of oxygen reached over 0.98 within 20 minutes. After 24 hours, all the surviving rats were killed by decapitation. Cerebral tissue was sliced and stained by haematoxylin-eosin and then enveloped. Brain tissue inju

关键词： volume fraction tissue injury nitric oxide synthase animal experiment result analysis neuronal injury cerebral cortex brain injury Wistar rats methods of method of

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The prevalence,characteristics and outcome of seizure in tuberculous meningitis

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Acta Epileptologica 2020年第1期2卷 1-9页

作者： Ammar Taha Abdullah Abdulaziz Jinmei Li Dong Zhou Department of Neurology West China HospitalSichuan University37 Guo Xue Xiang stChengdu 610041China. Faculty of Brain Sciences UCL Queen Square Institute of NeurologyLondon WC1N 3BGUK.

Seizures are a common finding in patients with tuberculous meningitis(TBM),and associate with four times increased risk of death and neurological disability,especially in *** has been reported that brain inflammation,diffuse neuronal injury,and reactive gliosis may all contribute to the pathogenesis of seizures in *** seizure onset may be associated with meningeal irritation and cerebral oedema;while,the late seizures are usually due to infarction,hydrocephalus,tuberculoma and paradoxical ***,recurrent uncontrolled seizures can evolve to status epileptics resulting in an increased risk of chronic epilepsy and poor ***,this review aimed to assess the frequency of seizures in patients with TBM,and discuss the etiologies,mechanisms,and characteristics of seizures in ***,we have searched the literature to identify the prognostic factors for chronic epilepsy after TBM.

关键词： Seizure Tuberculous meningitis neuronal injury Epilepsy

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Protection of neurons from hyperglycemia-induced injury by deletion of MAD2B

Protection of neurons from hyperglycemia-induced injury by d...

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中国神经科学学会第十届全国学术会议

作者： Xiao-Lan WANG Zhi-Hua YANG Guang-Pin CHU Xian-Fang MENG Department of Neurobiology School of Basic Medical SciencesTongji Medical CollegeHuazhong University of Science and Technology

Objective Diabetic encephalopathy may lead to cognitive deficits in diabetic patients and diminish quahty of *** has been shown that protracted hyperglycemia is directly associated with neuronal apoptosis,which is involved in diabetic ***1/APC is essential for the survival of postmitotic *** our previously study,we found that MAD2B,one of APC inhibitors,was expressed in neurons in central nervous ***,whether MAD2B is involved in hyperglycemia-induced apoptosis and thus takes part in diabetic encephalopathy is still *** To address this issue,we first explored the expression of MAD2B and cyclin Bl detected by immunofluorescence and Western blot in vivo and in vitro under *** further explore the role of MAD2B in hyperglycemia-induced neuronal injury,we depleted MAD2B expression by a specifically targeted shRNA against MAD2B in cultured *** we detected neuron apoptosis by TUNEL analysis and S phase with EdU *** It was found that hyperglycemia remarkably increased the expression of MAD2B and accumulation of cyclin Bl in cortices of diabetes mellitus rat model and in cultured primary *** results demonstrate that MAD2B expression is the main culprit for accumulation of cyclin B1 and apoptosis in neurons under high *** observed that MAD2B deficiency alleviated cyclin Bl expression and apoptotic neuronal ***,the increased expression of MAD2B promoted neurons to enter an aberrant S phase that led differentiated neurons into apoptotic cell *** These results suggest that hyperglycemia induced neuronal apoptosis through inducing expression of MAD2B,which represents a novel mechanism of diabetic encephalopathy.

关键词： Key ords:MAD2B hyperglycaemia cyclin B1 neuronal injury

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