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Intermittent hypoxia attenuates ischemia/reperfusion induced apoptosis in cardiac myocytes via regulating Bcl-2/Bax expression

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Cell Research 2003年第5期13卷 385-391页

作者： JIAN WEN DONG, HAI FENG ZHU, WEI ZHONG ZHU, HAI LEI DING, TIE MIN MA, ZHAO NIAN ZHOU 1 Laboratory of Hypoxic Cardiovascular physiology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, china.2 department of physiology and Pathophysiology, Health Science Center Peking University, Beijing 100083 china 1Laboratory of Hypoxic Cardiovascular physiology Shanghai Institutes for Biological SciencesChinese Academy of Sciences Shanghai 200031 China. E-mail: znzhou@*** 1Laboratory of Hypoxic Cardiovascular physiology Shanghai Institutes for Biological SciencesChinese Academy of Sciences Shanghai 200031 China. E-mail: znzhou@*** 1Laboratory of Hypoxic Cardiovascular physiology Shanghai Institutes for Biological SciencesChinese Academy of Sciences Shanghai 200031 China. E-mail: znzhou@*** 1Laboratory of Hypoxic Cardiovascular physiology Shanghai Institutes for Biological SciencesChinese Academy of Sciences Shanghai 200031 China. E-mail: znzhou@*** 1Laboratory of Hypoxic Cardiovascular physiology Shanghai Institutes for Biological SciencesChinese Academy of Sciences Shanghai 200031 China. E-mail: znzhou@*** 1Laboratory of Hypoxic Cardiovascular physiology Shanghai Institutes for Biological SciencesChinese Academy of Sciences Shanghai 200031 China. E-mail: znzhou@***

Intermittent hypoxia has been shown to provide myocardial protection against ishemia/reperfusion-induced injury. Cardiac myocyte loss through apoptosis has been reported in ischemia/reperfusion injury. Our aim was to investigate whether intermittent hypoxia could attenuate ischemia/reperfusion-induced apoptosis in cardiac myocytes and its potential mechanisms. Adult male Sprague-Dawley rats were exposed to hypoxia simulated 5000 m in a hypobaric chamber for 6 h/day, lasting 42 days. Normoxia group rats were kept under normoxic conditions. Isolated perfused hearts from both groups were subjected to 30 min of global ischemia followed by 60 min reperfusion. Incidence of apoptosis in cardiac myocytes was determined by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling （TUNEL） and DNA agarose gel electrophoresis. Expressions of apoptosis related proteins, Bax and Bcl-2, in cytosolic and membrane fraction were detected by Western Blotting. After ischemia/reperfusion, enhanced recovery of ca

关键词： intermittent hypoxia apoptosis cardiac myocytes Bax Bcl-2.

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A Type II Diabetic Model-from Insulin Resistance to Diabetes

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生物医学工程学杂志 2005年第S1期22卷 43-44页

作者： Yong WU~(1,2) Jing-Ping OU YANG~1 Jing-Fang ZHANG~1 Ke WU~11(department of Pathophysiology, Medical College of Wuhan University, Wuhan 430071, china)2(department of physiology, Hubei College of Traditional Chinese Medicine, Wuhan 430061, china)

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Neuroprotective effects of ginsenoside Rgl on the dopaminergic neuronsin the substantia nigra of MPTP-treated C57BL6 mice

Neuroprotective effects of ginsenoside Rgl on the dopaminerg...

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中国神经科学学会第四次会员代表大会暨第七届全国学术会议

作者： Hai-Dong YANG~1,Jun WANG~2,Hong JIANG~2,Jun- Xia XIE~(2*) 1 department of physiology,Medical College of Putian University,Putian 351100,china 2 department of physiology,Medical College of Qingdao University,Qingdao 266071,china

＜正＞In the present study,the effects of Ginsenoside Rgl（Rgl） on l-methy-4-phenyl-l,2,3,6-tetrahydropyridine （MPTP） induced dopamineregic neuron degeneration in the substantia nigra（SN） of C57BL6 mice were *** high-performance liquid chromatography electrochemical detection,we showed that the dopamine content in the striatum decreased after MPTP treatment,which could be restored by *** immunohistochemistry and semi-quantitative RT-PCR, we showed that Rgl could prevent the MPTP-induced decrease of tyrosine hydroxylase（TH） positive neurons and the TH mRNA expression in the substantia nigra（SN）.Further experiments demonstrated that Rg1 could reverse the changes of bax immunoreactive cells and the bax mRNA expression,bcl-2 immunoreactive cells and the bcl-2 mRNA expression as well as caspase-3 immunoreactive cells and the caspase-3 mRNA expression in the SN of MPTP treated mice. By Perls’ iron staining study we demonstrated that Rg1 prevented the MPTP-induced increase of iron-staining cells in the *** results suggested that the protective effects of Rg1 on the toxicity of MPTP could be attributed to its anti-apoptotic and iron- chelator-like properties.

关键词： Parkinson’s disease Ginsenoside Rg1 1-methy-4-pheny1-1,2,3,6-tetrahydropyridine(MPTP) dopamine apoptosis iron

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PRENATAL HYPOXIA STRESS INDUCED THE HIGH SENSITMTY OF HPA IN ADULT OFFSPRING RATS

PRENATAL HYPOXIA STRESS INDUCED THE HIGH SENSITMTY OF HPA IN...

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国际比较生理生化及毒理学大会暨第六届中国比较生理学会议

作者： J.M.Fan X.Q Chen~2 Jin Hao J.Z.Du~(1,2) 1 department of physiology,Divi.Neurobiology and physiology,College of Life Sciences,Zhejiang University,Zjjingang Campus,Hangzhou,310058,china 2 department of physiology,Divi.Neurobiology and physiology,School ofMedicine,Zhejiang University,Zijingang Campus,Hangzhou,310058,china

The present study set out to determine how prenatal hypoxia(embryonic hypoxia)affects the HPA axis and behavior in adult male *** regulating mechanisms were also *** rats were exposed either to intermittent hypoxic stress(simulated altitude of 5 kin,10.8% O,54.02 kPa), restraint stress,or the combination of both,daily for 4 hours throughout pregnancy(21 days).Normoxic

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Activation of corticotropin-releasing factor 2 receptor inhibits Purkinje neuron P-type calcium currents via Goa-dependent PKC eposilon pathway

Activation of corticotropin-releasing factor 2 receptor inhi...

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中国神经科学学会第四次会员代表大会暨第八届全国学术会议

作者： Jin TAO~(1 2 *) Yuan ZHANG~2 Hua HUANG~2 Xing-Hong JIANG~1 1 department of Neurobiology Medical College of Soochow University Suzhou 215123 china 2 department of physiology National University of Singapore 117597 Singapore

Corticotropin-releasing factor(CRF) receptors have been demonstrated to be widely expressed in the central nervous system and many peripheral tissues of ***,it is still unknown wheth

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Activation of corticotropin-releasing factor 2 receptor inhibits Purkinje neuron P-type calcium currents via Goa-dependent PKC eposilon pathway

Activation of corticotropin-releasing factor 2 receptor inhi...

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中国神经科学学会第四次会员代表大会暨第八届全国学术会议

作者： Jin TAO~(1,2,*),Yuan ZHANG~2,Hua HUANG~2,Xing-Hong JIANG~1 1 department of Neurobiology,Medical College of Soochow University,Suzhou 215123,china 2 department of physiology,National University of Singapore,117597 Singapore

Corticotropin-releasing factor(CRF) receptors have been demonstrated to be widely expressed in the central nervous system and many peripheral tissues of ***,it is still unknown whether CRF receptors will function in cerebellar Purkinje *** the present study,we investigated the expression profile of CRF receptors in rat cerebellum and identified a novel functional role of CRFR2 in modulating Purkinje neuron P-type Ca currents(P-currents). We found that CRFR2αmRNA,but not CRFR1 and CRFR2β,was endogenously expressed in rat *** of CRFR2 by UCN2 inhibited P-currents in a concentration-dependent manner(IC50～0.07μM).This inhibitory effect was abolished by astressin2B,a CRFR2 antagonist,and was blocked by GDP-β-S,pertussis toxin,or a selective antibody raised against the Goα.Inhibition of phospholipase C(PLC) blocked the inhibitory action of *** application of diacylglycerol(DAG) antagonist,1-hexadecyl-2-acetyl-sn-glycerol,as well as inhibition of either protein kinase C or its epsilon isoform(PKCε) abolished the UCN2 effect while 1-oleoyl-2-acetyl-sn-glycerol(EI-150),a membrane-permeable DAG analogue,occluded UCN2-mediated *** addition,UCN2 significantly increases spontaneous firing frequency of Purkinje neurons in cerebellar *** summary,activation of CRFR2 inhibits P-currents in Purkinje neurons via Goα-dependent PLC/PKCεpathway,which might contribute to its physiological functions in cerebellum.

关键词： P-type calcium channels Corticotropin-releasing factor receptor G-protein Purkinje neuron

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Proliferation and differentiation-inducing effects of aminosteroid H42648 on K562 leukemia cells

Proliferation and differentiation-inducing effects of aminos...

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湖南省生理科学会2006年度学术年会

作者： YIN Ya-ling~(1,2),HE Qun~(1,*) (1.Research Laboratory of Blood physiology,Xiangya School of Medicine,Central South University,Changsha 410078,china.2.department of physiology and Neurobiology,Xinxiang Medical College,Xinxiang 453003,china)

Objective To explore the proliferation and differentiation-inducing effects of aminosteroid H42648 on K562 leukemia *** The effects of H42648 on K562 cell proliferation were studied by cell count,colony count and MTT assay,the differentaition by morphology, benzidine stain and flow *** The growth of K562 cells was inhibited after treatment with H42648 for 5 *** inhibition rates for K562 cells in MTT assay were(26.90±3.18)%and(43.26±2.54)%respectively after treatment by 10mol/L and 10mol/L *** inhibition for K562 cells in colony culture assay were(22.21±9.20)%and(48.71±8.24)%at the dose of 10mol/L and 10mol/L H42648 respectively.H42648 also induced K562 cells toward erythroid *** was verified by bezindine stain in that the OD value at the dose of 10mol/L H42648 was increased by(153±17.65)% compared with the control,and at the dose of 10mol/L H42648 the OD value was increased by(250±4.60)%compare with the *** morphology showed the differetiation tendency after treatment of K562 *** from flow cytometry showed that after treatment with 10mol/L H42648 for 4 days,the percentage of positive CD71 expression in differentiated K562 cells was 89.91%.Conclusion H42648 can inhibit the proliferation of K562 cell lines and induce toward erythriod differetiation.H42648 may become a new lead for the differentiation-inducing therapy of leukemia.

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The response of P50 sensory gating in substantia Nigra on estrogen against dopaminergic neurons depleted by oxidative stress

The response of P50 sensory gating in substantia Nigra on es...

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中国神经科学学会第四次会员代表大会暨第七届全国学术会议

作者： Jinlan MENG~(1,2),Yuanyi MA~(1,3),Haiyun LUO~1,Min HE~(1*) 1 department of physiology,Kunming Medical College,Kunming,Yunnan 650031,china 2 department of physiology,Guangdong Pharmaceutical University,Guangzhou,Guangdong 510006,china 3 Fourth Military Medical University Press,Xian,Shanxi 710032,china

＜正＞Estrogen as a natural antioxidant of membrane phospholipids peroxidation can block the damage of dopaminergic neurons in substantia nigra（SN） lesioned by exotic toxicant like 6-hydroxydopamine（6-OHDA） to protect dopaminergic neurons in *** now researching the relationship between estrogen and the system of dopaminergic neurons in SN generally adopt ex vivo and acute animal microdialysis experiments which can not reflect estrogen’s internal proptection of antioxidative stress to dopaminergic neurons.A lot of substantial evidences strongly implied that P50 sensory gating （P50） and dopaminergic neurotransmitter have affinities,P50 can be recorded in a quite and awake *** the present P50 sensory gating in SN was studied in normal group（F-INT）,Parkinson’s disease model group with 6-OHDA lesioned SN（FPD）, ovariectomy + 6-OHDA Parkinson’s disease model group（F-OVX-PD） and ovariectomy + estrogen replacement + 6- OHDA Parkinson’s disease model group（F-OVX-E2-PD） to determine the change of P50 sensory gating in SN on estrogen against dopaminergic neurons depleted by oxidative stress.P50 auditory evoked potentials by two brief acoustic stimuli were recorded in the SN and the number of TH immunohistochemistry stained dopaminergic neurons in the SN was investigated after the determination of *** results demonstrated that:（1） The testing/conditioning（T/C） ratio of P50 is decreased significantly in F-PD group（0.399±0.074,n=15） as compared to F-INT group（0.667±0.037,n=21）（P＜0.01）;（2） The T/C ratio of P50 is decreased significantly in F-OVX-PD group（0.219±0.059,n=12） as compared to F-PD group and FOVX -E2-PD group（0.498±0.166,n=15）（P＜0.01）;（3） The T/C ratio of P50 is no difference between F-OVX-E2-PD group and F-PD group（P＞0.05）.（4） The number of TH+ cells in right SN（lesioned by 6-OHDA） of F-OVX-PD group decreased about 57.14%and 60.86%as compared to F-PD group and F-OVX-E2-PD group（P＜0.05）.The number of TH+ cells in right SN is decreased significantly as compared

关键词： P50 sensory gating estrogen dopaminergic neurons oxidative stress

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Phosphorylation of human Sgo1 by NEK2A is essential for chromosome congression in mitosis

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Cell Research 2007年第7期17卷 608-618页

作者： Guosheng Fu1 Xia Ding2,3 Kai Yuan1,2 Felix Aikhionbare2 Jianhui Yao1 Xin Cai1,2 Kai Jiang1,2 Xuebiao Yao1,21 Laboratory of Cellular Dynamics, Hefei National Laboratory, University of Science & Technology of china, Hefei 230027, china2 department of physiology and Cancer Biology Program, Morehouse School of Medicine, Atlanta, GA 30310, USA3 department of Medicine, Beijing University of Chinese Medicine, Beijing 100029, china Laboratory of Cellular Dynamics Hefei National Laboratory University of Science & Technology of China Hefei China. School of Biological Sciences University of Bristol Woodland Road Bristol BS8 1UG UK

Chromosome segregation in mitosis is orchestrated by the interaction of the kinetochore with spindle microtubules. Ourrecent study shows that NEK2A interacts with MAD1 at the kinetochore and possibly functions as a novel integrator ofspindle checkpoint signaling. However, it is unclear how NEK2 A regulates kinetochore-microtubule attachment in *** we show that NEK2A phosphorylates human Sgol and such phosphorylation is essential for faithful chromosomecongression in mitosis. NEK2A binds directly to HsSgol in vitro and co-distributes with HsSgol to the kinetochore ofmitotic cells. Our in vitro phosphorylation experiment demonstrated that HsSgol is a substrate of NEK2A and the phos-phorylation sites were mapped to Ser14and Ser507as judged by the incorporation of32P. Although such phosphorylation isnot required for assembly of HsSgol to the kinetochore, expression of non-phosphorylatable mutant HsSgol perturbedchromosome congression and resulted in a dramatic increase in microtubule attachment errors, including syntelic andmonotelic attachments. These findings reveal a key role for the NEK2A-mediated phosphorylation of HsSgol in orches-trating dynamic kinetochore-microtubule interaction. We propose that NEK2 A-mediated phosphorylation of human Sgolprovides a link between centromeric cohesion and spindle microtubule attachment at the kinetochores.

关键词： Sgo1 NEK2A phosphorylation microtubule kinetochore

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Humanin inhibited NMDA-MAPKs mediated excitotoxicity

Humanin inhibited NMDA-MAPKs mediated excitotoxicity

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中国神经科学学会第四次会员代表大会暨第八届全国学术会议

作者： Xiao-Rong YANG~1,Qi-Fang WENG~2,Peng-Jun ZHANG~1,Hua-Ping QIN~1,Ye WANG~1,Rui-Hong SHI~1,Ce ZHANG~(1,*) 1 department of physiology & Neurobiology,Shanxi Medical University,Taiyuan,030001,china 2 department of physiology,Hainan Medical College,Haikou 571101,china

Objective Humanin(HN) is a newly discovered peptide that was first isolated from brains of patients with Alzheimer’s disease(AD).Earlier studies focused on the neuroprotection of HN on AD-related ***,evidence has revealed that HN might have a broader spectrum of protective *** have multiple signaling pathways, including extracellular signal-regulated kinase(ERK),c-Jun N-terminal kinase(JNK) and p38 MAPK pathway,and each pathway varies from each other as for their physiological and pathological *** some reports have shown that the MAPK pathways indeed involved in NMDA-induced excitotoxicity,the contribution of each pathway is various in different models of toxic ***,influence of HN on MAPKs activities following NMDA treatment remained to be ***,the present study investigated the activation of the MAPK pathways by NMDA and the antagonism of *** Thus,we aimed to(1) Systematically investigate the contributions of ERK,JNK and p38 MAPK of the MAPK family to NMDA-mediated excitotoxicity(decrease of cell viability,evoked neuronal damage and cell death) of cortical neurons and observe the neuroprotection of HN against neuronal insults by using WST-8 assay,LDH levels assay and Calcein-AM staining,respectively;(2) Investigate the contribution of apoptosis in NMDA-induced excitotoxicity,characterize the contribution of each MAPK pathway related to NMDA-induced apoptosis and observe the neuroprotection of HN against apoptosis,as measured by caspase-3 activity,TUNEL staining and flow cytometry detection;(3) Based on the above studies,further elucidate the mechanisms or possible targets underlying the HN-mediated ***,observe the effect of HN on NMDA-induced change of intracellular calcium concentration by using calcium fluorescent image,and secondly clarify the activation of the three MAPK pathways by NMDA and the suppressive effects of HN by Western Blot ***(1) JNK inhibit

关键词： N-methyl-D-aspartate(NMDA) excitotoxicity mitogen-activated protein kinases(MAPKs) Humanin neuroprotection cortical neurons

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