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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

Huntingtin processing in pathogenesis of Huntington disease

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Acta Pharmacologica Sinica 2004年第10期 3-9页

作者： zheng-hong qin, zhen-lun gudepartment of pharmacology, soochow university school of medicine, suzhou 215 007, china Laboratory of Cellular Neurobiology, department of Neurology, Massachusetts General Hospital and Harvard Medical school, MA 02129, USA

Huntington's disease (HD) is caused by an expansion of the polyglutamine tract in the protein named huntingtin. The expansion of polyglutamine tract induces selective degeneration of striatal projection neurons and cortical pyramidal neurons. The bio-hallmark of HD is the formation of intranuclear inclusions and cytoplasmic aggregates in association with other cellular proteins in vulnerable neurons. Accumulation of N-terminal mutant huntingtin in HD brains is prominent. These pathological features are related to protein misfolding and impairments in protein processing and degradation in neurons. This review focused on the role of proteases in huntingtin cleavage and degradation and the contribution of altered processing of mutant huntingtin to HD pathogenesis.

关键词： Huntington disease huntingtin caspase calpain proteasome protein aggregation autophagy neurodegeneration

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

Effects of Xiaoyu tablet on blood lipid and lipoproteins in hyperlipidemic rabbits with atherosclerosis

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中华医学杂志(英文版) 2005年第19期000卷 69-71页

作者： XIE Mei-lin, gu zhen-lun and ZHU Lu-jiadepartment of pharmacology, Medical school of soochow university, suzhou 215007, china department of pharmacology Medical School of Soochow University Suzhou 215007 China

In general, low density lipoprotein (LDL), particularly oxidized-LDL, plays an important role in the occurrence and development of lipid-rich atheromatous plaque,~1 and the consequence is basis for plaque instability, rupture, and further complications.~ 2,3 And a high LDL-triglyceride level was related to progression of coronary atherosclerosis,~4 and the increments of serum triglyceride (TG) and LDL-triglyceride were risk factors for coronary artery disease.~ 5,6 Therefore, lipid-modifying therapy may have a beneficial effect on the prevention and treatment of atherosclerosis and its complications.~ 7,8 Because it is difficult to isolate and purify LDL, there are few data on total cholesterol (TC) and TG in LDL and consequently there is little information on the relationship between the lipid profile and levels of TC and TG in LDL. Xiaoyu tablet, a compound prepared from Chinese herbal medicines, consists of Radix Salviae Miltiorrhizae and Fructus Crataegi extracts. Our previous studies have demonstrated that the drug possesses the regulation of blood lipid and regression of atherosclerosis.~ 9-12 In this study, we observed the effects of Xiaoyu tablet on blood lipid, lipoproteins, and levels of TC and TG in LDL in atherosclerotic hyperlipidemic rabbits, and analysed their correlation and clinical significance.

关键词： hyperlipidemia · cholesterol · triglyceride · low density lipoprotein · high density lipoprotein

Development of novel therapies for Huntington's disease:hope and challenge

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Acta Pharmacologica Sinica 2005年第2期26卷 129-142页

作者： zheng-hong qin~(2,3,5),jin wang~4,zhen-lun gu~2~2department of pharmacology,soochow university school of medicine,suzhou 215007,china ~3Laboratory of Cellular Neurobiology,Massachusetts General Hospital and Harvard Medical school,Charlestown,MA 02129,USA ~4Molecular Neurogenetics Unit,Center forHuman Genetics Research,Massachusetts General Hospital and Harvard Medical school,Charlestown,MA 02129,USA departmentofpharmacology SoochowUniversitySchoolofMedicineSuzhou215007China

Huntington's disease(HD)is an autosomal dominant neurological *** is afatal neurological disorder affecting 5-10 out of 10000 *** there areintensive research efforts focusing on uncovering molecular mechanisms of thepathogenesis of HD,a number of studies have begun to look for effective thera-pies for *** is a large body of encouraging news on novel *** present paper reviews drugs used for symptomatic treatmentof HD and experimental therapies targeting HD molecular pathology.

关键词： Huntington disease huntingtin aggregates caspases nerve growth factors cell transplantation coenzyme Q10

Therapeutic effect of osthole on hyperlipidemic fatty liver in rats

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Acta Pharmacologica Sinica 2007年第3期28卷 398-403页

作者： Yan ZHANG Mei-lin XIE~2 Lu-jia ZHU zhen-lun gu department of pharmacology,Medical school of soochow university suzhou 215123,china departmentofpharmacology MedicalSchoolofSoochowUniversitySuzhou215123China

Aim:To study the effects of osthole on hyperlipidemic fatty liver and investigatethe possible ***:A rat model with hyperlipidemic fatty liverwas successfully established by feeding fatty milk for 6 *** experimentalrats were then treated with 5-20 mg/kg osthole for 6 *** mouse hyperlipi-demic model was induced by feeding fatty milk when they were treated with 10-20mg/kg osthole for 3 ***:After treatment with osthole,the levels of ratserum total cholesterol(TC),triglyceride(TG)and low density lipoprotein-choles-terol significantly decreased as compared with the fatty liver model group(P20 mg/kg osthole for 3 weeks(P<0.05 or P<0.01).Importantly,the histological evaluation of rat liver demonstrated that ostholedramatically decreased lipid accumulation(P<0.01).Conclusion:Osthole wasfound to have therapeutic effects on fatty milk-induced rat fatty liver;the mecha-nisms might be associated with its anti-oxidation and the elevation of the activi-ties of LPL and HL.

关键词： osthole hyperlipidemic fatty liver pharmacology

Dual roles of NF-kB in cell survival and implications of NF-kB inhibitors in neuroprotective therapy

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Acta Pharmacologica Sinica 2007年第12期 1859-1872页

作者： zheng-hong qin~(2,4,5),Lu-yang TAO~(3,4),Xin CHEN~(2,4)departments of ~2 pharmacology and ~3 Forensic medicine and ~4 Laboratory of Aging and Nervous Diseases,soochow university school ofmedicine,suzhou 215123,china

NF-kB is a well-characterized transcription factor with multiple physiological andpathological ***-kB plays important roles in the development andmaturation of lymphoids,regulation of immune and inflammatory response,andcell death and *** influence of NF-kB on cell survival could be protec-tive or destructive,depending on types,developmental stages of cells,and patho-logical *** complexity of NF-kB in cell death and survival derivesfrom its multiple roles in regulating the expression of a broad array of genesinvolved in promoting cell death and *** activation of NF-kB has beenfound in many neurological disorders,but its actual roles in pathogenesis are stillbeing *** compounds with neuroprotective actions are strongly as-sociated with the inhibition of NF-kB,leading to speculation that blocking thepathological activation of NF-kB could offer neuroprotective effects in certainneurodegenerative *** paper reviews the recent developments inunderstanding the dual roles of NF-kB in cell death and survival and explores itspossible usefulness in treating neurological *** paper will summarizethe genes regulated by NF-kB that are involved in cell death and survival toelucidate why NF-kB promotes cell survival in some conditions while facilitatingcell death in other *** paper will also focus on the effects of variousNF-kB inhibitors on neuroprotection in certain pathological conditions to specu-late if NF-kB is a potential target for neuroprotective therapy.

关键词： NF-kB transcription factor apoptosis neuroprotection neurodegeneration

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