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Food Science and Human Wellness 2020年第3期9卷 264-271页

作者： Xiyun Sun Zihan Xu Yuehua Wang Ning Liu College of Food Shenyang Agricultural University120 Dongling RdShenyang City 110866China College of Land and Environment Shenyang Agricultural UniversityChina

The protective effects of blueberry anthocyanin extracts against damage induced by extremely lowfrequency electromagnetic field(ELF-EMF)were investigated in a rat *** rats were exposed to ELF-EMF with or without the administration of blueberry anthocyanin extracts(50,100,and 200 mg/kg per day intragastrically once a day)for 30 *** anthocyanin extracts supplementation inhibited the decrease in Nissl substance levels,cell membrane integrity,and mitochondrial membrane potential induced by ELF-EMF;prevented the increase in nitric oxide,malondialdehyde,and Ca2+concentrations;suppressed superoxide dismutase and glutathione depletion;and enhanced the cognitive ability of the rats exposed to *** protective effects of blueberry anthocyanin extracts against hippocampal neuron injury caused by ELF-EMF were *** results demonstrated that blueberry anthocyanin extracts suppress hippocampal neuron injury caused by ELF-EMF by inhibiting cell membrane damage and oxidative stress pathways,and suggested that blueberry anthocyanin treatment potentially prevents hippocampal neuron injury.

关键词： Blueberry anthocyanin extracts Protective effects Extremely low-frequency electromagnetic field hippocampal neuron

L-Type Calcium Channel Modulates Low-Intensity Pulsed Ultrasound-Induced Excitation in Cultured hippocampal neurons

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Neuroscience Bulletin 2024年第7期40卷 921-936页

作者： Wen-Yong Fan Yi-Ming Chen Yi-Fan Wang Yu-Qi Wang Jia-Qi Hu Wen-Xu Tang Yi Feng Qian Cheng Lei Xue State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science Fudan UniversityShanghai 200433China Department of Physiology and Neurobiology School of Life SciencesFudan UniversityShanghai 200438China Institute of Acoustics School of Physics Science and EngineeringTongji UniversityShanghai 200092China Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education Tongji UniversityShanghai 200070China Center for Rehabilitation Medicine Department of Pain ManagementZhejiang Provincial People's HospitalAffliated People's HospitalHangzhou Medical CollegeHangzhou 310014China Department of Critical Care Medicine Shanghai General HospitalShanghai Jiaotong University School of MedicineShanghai 200080China Shanghai Research Institute for Intelligent Autonomous Systems Tongji UniversityShanghai 201210China Research Institute of Intelligent Complex Systems Fudan UniversityShanghai 200433China

As a noninvasive technique,ultrasound stimulation is known to modulate neuronal activity both in vitro and in *** latest explanation of this phenomenon is that the acoustic wave can activate the ion channels and further impact the electrophysiological properties of targeted ***,the underlying mechanism of low-intensity pulsed ultrasound(LIPUS)-induced neuro-modulation effects is still ***,we characterize the excitatory effects of LIPUS on spontaneous activity and the intracellular Ca^(2+)homeostasis in cultured hippocampal *** whole-cell patch clamp recording,we found that 15 min of 1-MHz LIPUS boosts the frequency of both spontaneous action potentials and spontaneous excitatory synaptic currents(sEPSCs)and also increases the amplitude of sEPSCs in hippocampal *** phenomenon lasts for>10 min after LIPUS *** with Ca^(2+)imaging,we clarified that LIPUS increases the[Ca^(2+)]cyto level by facilitating L-type Ca^(2+)channels(LTCCs).In addition,due to the[Ca^(2+)]cyto elevation by LIPUS exposure,the Ca^(2+)-dependent CaMKII-CREB pathway can be activated within 30 min to further regulate the gene transcription and protein *** work suggests that LIPUS regulates neuronal activity in a Ca^(2+)-dependent manner via *** may also explain the multi-activation effects of LIPUS beyond *** stimulation potentiates spontaneous neuronal activity by increasing Ca^(2+)influx.

关键词： Low-intensity pulsed ultrasound Neuromodulation L-type calcium channel hippocampal neuron

Astragalus injection inhibits c-Jun N terminal kinase mRNA expression following oxygen-glucose deprivation and reintroduction in rat hippocampal neurons

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Neural Regeneration Research 2009年第11期4卷 879-884页

作者： Dongqing Ye Weijuan Gao Fengxia Yan Tao Qian Yali Zhang Research Room of Pathophysiology Chengde Medical College Chengde 067000 Hebei Province China Affiliated Hospital of Chengde Medical College Chengde 067000 Hebei Province China

BACKGROUND： In studies concerning cell injury induced by cerebral ischemia-reperfusion, current experiments have primarily focused on altered protein levels. In addition, the apoptotic proteins Bax and Bcl-2 have been thoroughly studied with regard to initiating neuronal apoptosis. OBJECTIVE： To establish an in vitro model of oxygen-glucose deprivation and reintroduction in the rat hippocampus to simulate cerebral ischemia-reperfusion injury; to observe c-Jun N-terminal kinase 3 （JNK3） mRNA expression in hippocampal neurons following Astragalus injection; and thus to determine changes in the signaling and downstream pathways of neuronal apoptosis at the cellular and molecular level. DESIGN, TIME AND SETTING： A randomized, controlled, cellular and molecular experiment was performed at the Department of Central Laboratory, Chengde Medical College from February to June 2008. MATERIALS： Astragalus injection, the main ingredient of astragaloside, was purchased from Chengdu Di＇ao Jiuhong Pharmaceutical Manufactory, China. JNK3 mRNA probe and in situ hybridization kit were purchased from Tianjin Haoyang Biological Technology, China, and JNK3 RT-PCR primers were designed by Shanghai Bio-engineering, China. METHODS： Primary cultures of hippocampal neurons derived from Sprague Dawley rats, aged 1 2 days, were established. After 8 days, the hippocampal neurons were assigned to the following interventions： model group, Astragalus group, and vehicle control group, cells were subjected to oxygen-glucose reintroduction after oxygen-glucose deprivation for 30 minutes in sugar-free Earle＇s solution and a hypoxia device, which contained high-purity nitrogen. The normal control group was subjected to primary culture techniques and was not treated using above-mentioned interventions. In addition, the Astragalus and vehicle control groups were treated with Astragalus injection （0.5 g/L raw drug） or sterile, deionized water at 2 hours prior to oxygen-glucose deprivation, respectively. MA

关键词： oxygen-glucose deprivation and reintroduction Astragalus injection c-jun N-terminalkinase 3 mRNA hippocampal neuron

Selenocysteine antagonizes oxygen glucose deprivation-induced damage to hippocampal neurons

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Neural Regeneration Research 2018年第8期13卷 1433-1439页

作者： Xian-Jun Wang Mei-Hong Wang Xiao-Ting Fu Ya-Jun Hou Wang Chen Da-Chen Tian Su-Yun Bai Xiao-Yan Fu Department of Neurology People's Hospital of Linyi Linyi Shandong Province China Department of Neurology People's Hospital of Yishui Linyi Shandong Province China School of Basic Medicine Taishan Medical University Taian Shandong Province China

Designing and/or searching for novel antioxidants against oxygen glucose effective strategy for the treatment of human isdlemic stroke. Selenium is deprivation （OGD）-induced oxidative damage represents an an essential trace dement, which is beneficial in the chemo- prevention and chemotherapy of cerebral ischemic stroke. The underlying mechanisms for its therapeutic effects, however, are not well documented. Selenocysteine （SeC） is a selenium-containing amino acid with neuroprotective potential. Studies have shown that SeC can reduce irradiation-induced DNA apoptosis by reducing DNA damage. In this study, the in vitro protective potential and mechanism of action of SeC against OGD-induced apoptosis and neurotoxicity were evaluated in HT22 mouse hippocampal neurons. We cultured HT22 cells in a glucose-free medium containing 2 mM Na2S402, which formed an OGD environment, for 90 minutes. Findings from MTT, flow cytometry and TUNEL staining showed obvious cytotoxicity and apoptosis in HT22 cells in the OGD condition. The activation of Caspa se-7 and Caspase-9 further revealed that OGD-induced apoptosis of HT22 cells was mainly achieved by triggering a mitochondrial-medi- ated pathway. Moreover, the OGD condition also induced serious DNA damage through the accumulation of reactive oxygen species and superoxide anions. However, SeC pre-treatment for 6 hours effectively inhibited OGD-induced cytotoxicity and apoptosis in HT22 cells by inhibiting reactive oxygen species-mediated oxidative damage. Our findings provide evidence that SeC has the potential to suppress OGD-induced oxidative damage and apoptosis in hippocampal neurons.

关键词： selenium selenocysteine ischemic stroke oxygen glucose deprivation hippocampal neuron mitochondria reaction oxygen species superoxide anion oxidative damage apoptosis

Effect of New O-Superfamily Conotoxin on Voltage-Activated Currents of hippocampal neurons

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Tsinghua Science and Technology 2004年第1期9卷 64-68页

作者：李湛何湘平戴秋云黄培堂谢佐平 Department of Biological Sciences and Technology Tsinghua University Beijing 100084 China Institute of Biotechnology Beijing 100071 China

The effects of a new O-superfamily conotoxin, SO3, on sodium current (INa), transient A-type potassium currents (IA),and delayed rectified potassium currents (IK), were examined in cultured rat hippocampal neurons using the whole-cell patch clamp technique. Addition of SO3 caused a concentration-dependent, rapidly developing, and reversible inhibition of voltage-activated currents. The IC50 values for the blockage of INa , IA, and IK were calculated as 0.49, 33.9, and 7.6 mmol/L, respectively. The determined Hill coefficients were 1.7, 0.6, and 1.2, respectively. These results indicate that SO3 can selectively inhibit neuronal sodium and potassium currents.

关键词： hippocampal neuron patch-clamp SO3 sodium current potassium current

Effect of Yiqi Bushen prescription on hippocampal neuronal apoptosis in diabetic rats

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Neural Regeneration Research 2011年第21期6卷 1628-1634页

作者： Deshan Liu Weiwei Lin Wei Gao Ping Chang Wei Li Department of Traditional Chinese Medicine Qilu Hospital of Shandong University Jinan 250012 Shandong Province China

This study investigated the neuroprotective effect of Yiqi Bushen prescription （YQBS, supplementing qi and tonifying kidney） on neuronal cell apoptosis. Following YQBS treatment, the number of surviving hippocampal neurons increased, anti-apoptotic Bcl-2 expression increased and pro-apoptotic Bax expression decreased. In addition, diabetic rats exhibited improved learning and memory. YQBS treatment also increased Bcl-2 mRNA expression and the ratio of Bcl-2/Bax, but decreased levels of hypoxia-inducible factor-1α mRNA and Bax mRNA expression after high-glucose/hypoxia-induced injury. Results demonstrated that YQBS inhibited hippocampal neuronal apoptosis by decreasing hypoxia-inducible factor-1α expression and increasing Bcl-2 expression, thereby improving cognitive impairment in diabetic rats.

关键词： Yiqi Bushen prescription hippocampal neuron hypoxia-inducible factor-1α apoptosis diabetes learning and memory neural regeneration

Influence of Ginkgo Biloba extract on beta-secretase in rat hippocampal neuronal cultures following chronic hypoxic and hypoglycemic conditions

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Neural Regeneration Research 2008年第10期3卷 1065-1069页

作者： Xueneng Guan Fuling Yan Department of Neurology Jiangsu Provincial Institute of Traditional Chinese Medicine Nanjing 210038 Jiangsu Province China Department of Neurology Zhongda Hospital Southeast University Nanjing 210009 Jiangsu Province China

BACKGROUND： Preparation of Ginkgo leaf has been widely used to improve cognitive deficits and dementia, in particular in Alzheirner＇s disease patients. However, the precise mechanism of action of Ginkgo leaf remains unclear. OBJECTIVE： To explore the effect of Ginkgo Biloba extract （Egb761）, Ginaton, on β -secretase expression in rat hippocampal neuronal cultures following chronic hypoxic and hypoglycemic conditions. DESIGN, TIME AND SETTNG： Completely by randomized, grouping study. The experiment was performed at the Laboratory of Molecular Imaging, Southeast University between August 2006 and August 2007. MATERIALS： A total of 128 Wistar rats aged 24 hours were selected, and hippocampal neurons were harvested for primary cultures. METHODS： On day 7, primary hippocampal neuronal cultures were treated with Egb761 （0, 25, 50, 100, 150, and 200μg/mL） under hypoxic/hypoglycemic or hypoglycemic culture conditions for 12, 24, and 36 hours, respectively. hippocampal neurons cultured in primary culture medium served as control. MAIN OUTCOME MEASURES： Cell viability was assayed using 3-（4,5-Dimethylthiazol-2-yl）- 2,5-diphenyltetrazolium bromide （MTT）; fluorescence detection of β -secretase activity was performed; Western Blot was used to measure β -secretase expression. RESULTS： Cell viability under hypoxic/hypoglycemic or hypoglycemic culture conditions was significantly less than control cells （P 〈 0.05）. Under hypoxic/hypoglycemic or hypoglycemic culture conditions, treatment with 25 μg/mL Egb761 did not alter cell viability. However, 〉 25 μg/mL Egb761 induced greater cell viability （P 〈 0.05）. No differences were observed between hypoxic/hypoglycemic or hypoglycemic cells （P 〉 0.05）. α -secretase activity was increased after 12 hours in hypoxic/hypoglycemic culture （P 〈 0.01）. There were no significant differences between the 12-, 24-, or 36-hour Egb761 groups and the hypoxic/hypoglycemic groups （P 〉 0.05）. β -secretase activity was greater after 12, 24, and 36 hours in

关键词： α -secretase β -secretase Alzheirner's disease chronic hypoxia hippocampal neuron hypoglycemia

Role of chloride channels in nitric oxide-induced rat hippocampal neuronal apoptosis in vitro

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Neural Regeneration Research 2010年第9期5卷 690-694页

作者： Quanzhong Chang Shuling Zhang Jinbao Yin Department of Physiology Zhuhai Campus of Zunyi Medical College Zhuhai 519041 Guangdong Province China

BACKGROUND：Chloride channels participate in non-neuronal ***,it remains unclear whether chloride channels are involved in ischemic neuronal ***：To explore the effects of 4-acetamido-4＇-isothiocyanatostilbene-2,2＇-disulfonic acid （SITS） and 4,4＇-diisothiocyanostilbene-2,2＇-disulfonic acid （DIDS）,two chloride channel blockers,on the hippocampal neuronal apoptosis induced by 3-morpholinosydnonimine （SIN-1） based on the nitric oxide toxicity theory of neuronal apoptosis following ischemic brain ***,TIME AND SETTING：Comparative observation and in vitro experiments were performed at the laboratory of Zhuhai Campus of Zunyi Medical College from January to May ***：SIN-1,SITS,and DIDS were purchased from Sigma,***：hippocampal neurons from Sprague-Dawley rats,aged 1 day,were cultured In vitro for 12 days and randomly assigned to control,SIN-1,or chloride channel blocker ***-1 group neurons were induced by SIN-1 for 18 hours to establish a model of ischemic neuronal *** in chloride channel blocker groups were treated with SITS or DIDS plus SIN-1 for 18 *** controls were cultured in DMEM/Ham＇s F12 complete medium *** OUTCOME MEASURES：The apoptotic neurons and nuclear appearance were detected by Hoechst 33258 fluorescence staining; neuronal viability was quantitatively determined by 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide ***-3 activity was analyzed by Western ***：SIN-1 （1 mmol/L） dramatically induced apoptosis （50%-60%）.SITS and DIDS inhibited nitric oxide-induced neuronal injury in a dose-dependent manner,suppressed caspase-3 activation,reduced neuronal apoptosis,and improved neuronal ***：Chloride channel blockers can protect against neuronal injury induced by *** channels might be involved in neuronal apoptosis following cerebral ischemia.

关键词： chloride channel nitric oxide hippocampal neuron rats cerebral ischemia neural regeneration

Hypoxia induces an increase in intracelluar magnesium via TRPM7 channels in rat hippocampal neurons in vitro

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Hypoxia induces an increase in intracelluar magnesium via TR...

Mitochondrial BNIP3 upregulation precedes endonuclease G translocation in hippocampal neuronal death following oxygen-glucose deprivation

中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Xiuying CHEN,Jing ZHANG,Fengbo ZHAO,Yin ZHAO,Lei PEI,Ning SUN,Jing SHI~* Department of Neurobiology and Key Laboratory of Neurological Disease of Hubei Province,Tongji Medical College, Huazhong University of Science and Technology,13 Hangkong Road,Wuhan 430030,China

Objective TRPM7,as a divalent cation channel plays an important role in neurons damaged from cerebral ischemia due to permitting intracellular calcium *** study aimed to explore whether magnesium was transported via TRPM7 channel into intracellular space of rat hippocampal *** After 1 hour oxygenglucose deprivation(OGD) and acute chemical ischemia(CI) by using methods of Mg fluorescent probe Mag-Fura -2 to detect intracellular magnesium concentration([Mg]) and flame atomic absorption spectrometry to measure extracellular magnesium concentration([Mg]).Results The results showed that the neuronal[Mg];was as 1.51 fold high after 1 h OGD as basal level and the increase of neuronal[Mg] reached the peak after 1 h OGD and kept on for 60 min within *** the[Mg] decreased after 1 h OGD and recovered to the pre-ischemic level within 15 min after *** the situation of CI,the[Mg] peak immediately appeared in hippocampal *** increase of[Mg] was declined by removing extracellular magnesium in OGD or ***, using Gd or 2-APB to inhibit TRPM7 channels,[Mg] increase which induced by OGD or CI was attenuated without altering basal level of[Mg].By silencing TRPM7 with shRNA in hippocampal neurons,it was found that not only the increase of[Mg] induced by OGD or CI but also the basal level of[Mg] were *** contrast, overexpression of TRPM7 in HEK293 cells exaggerated both the basal and increased[Mg] after 1 h OGD/CI. Conclusion Results suggest that anoxia induce increase of[Mg] via TRPM7 channels in rat hippocampal neurons.

关键词： hippocampal neuron HEK293 cell oxygen-glucose deprivation TRPM7 magnesium homeostasis

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Mitochondrial BNIP3 upregulation precedes endonuclease G tra...