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Caspase-1 inhibitor Ac-YVAD-CHO attenuates quinolinic acid-induced increases in p53 and apoptosis in rat striatum

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Acta Pharmacologica Sinica 2005年第2期26卷 150-154页

作者： Yi CAO zhen-lun GU Fang LIN Rong HAN zheng-hong qin Department of pharmacology,soochow university school of medicine,suzhou 215007,china Department of pharmacology Soochow University School of Medicine Suzhou 215007 China

Aim:To study the effects of the caspase-1 inhibitor Ac-YVAD-CHO on quinolinicacid(QA)-induced ***:Rats were pre-treated with intrastriatalinfusion of Ac-YVAD-CHO(2-8μg)before intrastriatal injection of QA(60 nmol).Striatal total proteins,genomic DNA,and nuclear proteins were *** of Ac-YVAD-CHO on QA-induced caspase-1 activity,internucleosomalDNA fragmentation, IκB-α degradation,NF-κB,and AP-1 activation,and increasesin p53 protein levels were measured with enzyme assays,agarose gel electro-phoresis,electrophoresis mobility shift assays,and Western blot ***:Pre-treatment with Ac-YVAD-CHO inhibited QA-induced internucleo-somal DNA ***-YVAD-CHO inhibited QA-induced increases incaspase-1 activity and p53 protein levels,but had no effect on QA-induced IκB-αdegradation,NF-κB or AP-1 ***:Caspase-1 is involved inQA-induced p53 upregulation but not IκB-α *** of caspase-1attenuates QA-induced apoptosis in rat striatum.

关键词： caspase 1 Ac-YVAD-CHO Huntington disease protein p53 NF-kappaB inhibitor alpha apoptosis NF-kappaB

Prostaglandin A1 inhibits increases in intracellular calcium concentration,TXA2 production and platelet activation

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Acta Pharmacologica Sinica 2006年第5期27卷 549-554页

作者： Yi ZHU zhen-lun GU Zhong-qin LIANG Hui-lin ZHANG zheng-hong qin~2 Department of pharmacology,soochow university school of medicine,suzhou 215123,china Departmentofpharmacology SoochowUniversitySchoolofMedicineSuzhou215123China

Aim:In our previous studies we found that cyclopentenane prostaglandin A1(PGA1) had neuroprotective effects in a rodent ischemic *** the presentstudy we aimed to investigate the inhibitory effect of PGA1 on platelet ***:The rate of aggregation of human platelets was measured by *** rate of adhesion of platelets to cultured endothelial cells wasdetermined by using [~3H]-adenine labeled platelets.5-Hydroxytryptamine releasefrom platelets was measured with O-phthaldialdehyde *** levels of TXB2,a stable metabolite of TXA2,were determined by *** in platelet morphology were observed using an electronmicroscope,and the intraplatelet free calcium concentrations were measured withFluo-3/AM FCM ***:PGA1 significantly inhibited thrombin-,col-lagen-and ADP-induced aggregation and adhesion of *** morphologi-cal changes of platelets induced by thrombin were blocked by ***1inhibited the release of 5-hydroxytyptamine from dense granules and the synthe-sis of ***:PGA1 inhibits the activation of platelets probablythrough blocking increases in intracellular calcium concentration and TXA2synthesis.

关键词： prostaglandin A1 platelet aggregation calcium TXA2

Quality Control System of the Endoplasmic Reticulum and Related Diseases

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Acta Biochimica et Biophysica Sinica 2006年第4期38卷 219-226页

作者： Jun-Chao WU Zhong-qin LIANG zheng-hong qin* Department of pharmacology,school of medicine,soochow university,suzhou 215123,china Departmentofpharmacology SchoolofMedicineSoochowUniversitySuzhou215123China

The quality control (QC) system of the endoplasmic reticulum (ER) is an important monitoringmechanism in the protein maturation process,which ensures export of properly folded proteins from the *** or incompletely folded proteins are retained in the ER for refolding or degradation by the ER-residing *** calnexin/calreticulin cycle and ER-associated degradation are the key elements *** two mechanisms work together to allow incorrectly folded proteins have additional opportunitiesto achieve their native *** QC dysfunction is involved in many diseases caused by mutantproteins,many of which are causes of neurodegenerative disorders.A better understanding of molecularregulation in the QC system will uncover the molecular pathogenic mechanisms of many diseases caused byprotein misfolding and help discover novel strategies for preventing or treating these diseases.

关键词： protein folding quality control calnexin/calreticulin cycle endoplasmic reticulum-associated degradation protein misfolding disease

Molecular mechanism and regulation of autophagy

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Acta Pharmacologica Sinica 2005年第12期26卷 1421-1434页

作者： Ya-ping YANG~2 Zhong-qin LIANG~2 zhen-lun GU~2 zheng-hong qin~(2,3) 2 Department of pharmacology,soochow university school of medicine,suzhou 215007,china Departmentofpharmacology SoochowUniversitySchoolofMedicineSuzhou215007China

Autophagy is a major cellular pathway for the degradation of long-lived pro-teins and cytoplasmic organelles in eukaryotic cells.A large number of intracellu-lar/extracellular stimuli,including amino acid starvation and invasion ofmicroorganisms,are able to induce the autophagic response in *** discov-ery of the ATG genes in yeast has greatly advanced our understanding of themolecular mechanisms participating in autophagy and the genes involved in regu-lating the autophagic *** yeast genes have mammalian homologs,suggesting that the basic machinery for autophagy has been evolutionarily con-served along the eukaryotic *** regulation of autophagy is a very com-plex *** signaling pathways,including target of rapamycin(TOR)ormammalian target of rapamycin(mTOR),phosphatidylinositol 3-kinase-I(PI3K-I)/PKB,GTPases,calcium and protein synthesis all play important roles in *** molecular mechanisms and regulation of autophagy are dis-cussed in this review.

关键词： autophagy phosphatidylinositol 3-kinase Atg protein mTOR protein protein degradation

Animal models of Huntington's disease: implications in uncovering pathogenic mechanisms and developing therapies

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Acta Pharmacologica Sinica 2006年第10期27卷 1287-1302页

作者： Lin-hui WANG~2 zheng-hong qin~(3,4) Departments of ~2Physiology and ~3pharmacology,soochow university school of medicine,suzhou 215123,china DepartmentsofPhysiologysoochowuniversityschoolofmedicine Suzhou215123China Departmentsofpharmacology SoochowUniversitySchoolofMedicineSuzhou215123China

Huntington’s disease (HD) is an autosomal dominant neurodegenerative disorder,which is caused by an abnormal expansion of Cytosine Adenine Guanine (CAG)trinucleotide repeat in the gene making huntingtin (Htt).Despite intensiveresearch efforts devoted to investigate molecular mechanisms of pathogenesis,effective therapy for this devastating disease is still not available at *** of various animal models of HD has offered alternative approachesin the study of HD molecular *** HD models,including chemical-induced models and genetic models,mimic some aspects of HD symptoms *** date,however,there is no ideal model which replicates all of theessential features of neuropathology and progressive motor and cognitive impair-ments of human *** a result,our understanding of molecular mechanisms ofpathogenesis in HD is still limited.A new model is needed in order to uncover thepathogenesis and to develop novel therapies for *** this review we discussedusefulness and limitations of various animal and cellular models of HD in uncov-ering molecular mechanisms of pathogenesis and developing novel therapies forHD.

关键词： Huntington’s disease huntingtin neurodegeneration animal models

Potential applications of cyclopentenane prostaglandins in cardiovascular and cerebrovascular diseases

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Potential applications of cyclopentenane prostaglandins in c...

Neuroprotective effects of prostaglandin A1 and its inhibitory effect on NF-κB signaling pathway in rat models of permanent focal cerebral ischemia

11th International Vascular Neuroeffector Mechanisms and Cardiovascular pharmacology and medicine Symposia, Shanghai-suzhou 2006

作者： zheng-hong qin Department of pharmacology, soochow university school of medicine, suzhou 215123

Cyclopentenone prostaglandins (cycPG) including A and J series are formed from the enzyme-induced dehydration of prostaglandin E and D. They have some unique biological activities that are different from those of classic prostaglandins. PGA1 and PGJ2 affect multiple signaling pathways including inhibition of NF-κB activation, activation of peroxisome

关键词： Potential applications of cyclopentenane prostaglandins in cardiovascular and cerebrovascular diseases

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Neuroprotective effects of prostaglandin A1 and its inhibito...

Huntingtin Cleavage Induced by Thrombin In Vitro

中国神经科学学会第六届学术会议暨学会成立十周年庆祝大会

作者： Zhang Hui-ling, Gu zhen-lun , qin zheng-hong Department of pharmacology, soochow university school of medicine, suzhou 215007

Objective: Prostaglandin A1 (PGA1) is a cyclopentenone prostaglandin. Recently, we reported that PGA1 can inhibit excitotoxin-induced apoptosis of striatal neurons in vivo and rotenone-induced apoptosis of cultured SH-SY5Y cells, suggesting that PGA1 may have neuroprotective efficacy, possibly mediated by inhibition of NF-κB activation. The present study evaluated the neuroprotective potential of PGA1 and its effect on NF-κB signaling pathway in rat models of permanent focal cerebral ischemia. Methodes: Permanent middle cerebral artery occlusion (pMCAO) model was constructed by intraluminal

关键词： prostaglandin Al cerebral ischemia NF-κB

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Acta Biochimica et Biophysica Sinica 2007年第1期39卷 15-18页

作者： Fang LIN Junchao WU Yan WANG and zhenghong qin Department of pharmacology,Laboratory of Aging and Nervous Diseases,soochow university school of medicine,suzhou 215123,china Department of pharmacology Laboratory of Aging and Nervous DiseasesSoochowUniversity School of MedicineSuzhou 215123China

Huntingtin (Htt) mutation causes Huntington's *** analysis of Htt revealed apossible thrombin cleavage site in the N-terminal region of *** order to investigate if thrombin can eleaveHtt,we expressed the N-terminal fragment (1-969) of wild-type (wt) Htt (Htt 1-969) in MCF-7 cells andstudied its cleavage pattern by thrombin in *** expression plasmid pcDNA3-Htt-18Q-969 was used totransfect MCF-cells and Htt 1-969 expression was confirmed with *** lysates wereincubated with thrombin (1 U/ml, 10 U/ml,and 30 U/ml) for 1 h in the presence or absence of hirudin,athrombin *** fragments were separated by sodium dodecylsulfate-polyacrylamide gel electrophoresis(SDS-PAGE) and detected with anti-Htt antibodies. An Htt fragment with molecular mass of approximately80 kDa was produced after incubation with *** size of this Htt fragment was anticipated bymolecular mass generated from thrombin-mediated cleavage at the amino acid 183 in the *** ofan 80 kDa fragment was inhibited by hirudin. This study provides the first evidence that Htt is cleaved bythrombin in vitro at amino acid *** endogenous thrombin cleaves Htt in vivo,the physiological significanceof thrombin-mediated cleavage of Htt should be further investigated.

关键词： thrombin huntingtin(Htt) cleavage hirudin

AICAR-based exercise mimetic alleviates aging-induced memory impairment through activating AMPK and improving mitochondrial quality control

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Food Science and Human Wellness 2024年

作者： Bo Liao Yuan-Yuan qin Shan-Yao Pan Gui-Ping Wang Zhi Jiang Bin Li Yao Wang Yu-Long Wang Ming-Chao Zhou Yong Zhang Gang Liu zheng-hong qin Xue-Feng Xi Li Luo Department of pharmacology and Laboratory of Aging and Nervous Diseases (SZS0703) Jiangsu Key Laboratory of Translational Research and Therapy for NeuroPsycho-Diseases， soochow university school of Pharmaceutical Science College of Physical Education， Henan university school of Physical Education and Sports Science， soochow university Department of Pharmacy， suzhou Hospital of Traditional Chinese medicine suzhou TCM Hospital Affiliated to Nanjing university of Chinese medicine Laboratory Animal Center， Medical College of soochow university Center Lab of Ninth People's Hospital of suzhou Department of Rehabilitation medicine， Nan‘ao People's Hospital of Dapeng New District Rehabilitation Department， The First Affiliated Hospital of Shenzhen university， Shenzhen Second People's Hospital Tianjin Key Lab of Exercise Physiology and Sports medicine， Tianjin university of Sport Department of Rehabilitation medicine， Nanfang Hospital， Southern Medical university

Growing evidence suggests that exercise can provide neuroprotection by improving mitochondrial quality control (MQC) on the aged brain. Adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) signaling responsiveness declines with aging. However， whether AMPK plays a role in the exercise-mediated improvement of memory and MQC in the aged hippocampus remains to be established. AICAR (5-Aminoimidazole 4-carboxamide ribonucleoside)， a pharmacological agonist of AMPK， has been proposed to be an exercise mimetic recently. However， it has not been clarified whether AICAR could mimic the effects of exercise on the aged hippocampus through improvement of MQC. In this study， AICAR (AMPK agonist) and Compound C (AMPK inhibitor) were used to investigate if AMPK plays a key role in exercise-induced improvement of MQC and if AICAR could act as an exercise mimetic through improvement of MQC in aged hippocampus. Both exercise and AICAR improved the memory of aged mice and increased AMPK phosphorylation in the aged hippocampus. Exercise， but not AICAR， improved mitochondrial respiratory function in the aged hippocampus and increased the Microtubule associated protein 1 light chain 3 (LC3) II/LC3 I ratio and the protein expression of LC3 II and Autophagy Related Protein 7 (ATG7) in the lysate of whole hippocampal tissue. Both exercise and AICAR increased the ratio of LC3 II/LC3 I and the protein expression of LC3 II in the mitochondrial fractions of the hippocampus. Regarding mitochondrial dynamics， neither exercise training nor AICAR changed the protein level of Mitofusin2 (Mfn2). Exercise， but not AICAR， increased the protein level of Dynamin-related protein 1 (Drp1). Furthermore， both exercise training and AICAR increased the protein level of peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α)， a modulator of mitochondrial biogenesis. Compound C abolished the exercise-induced effects on memory in aged mice (Fig. 1)， AMPK phosphorylation， autophagy， mitop

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