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Nitric oxide modulates hypoxic pulmonary smooth muscle cell proliferation and apoptosis by regulating carbon monoxide pathway

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Acta Pharmacologica Sinica 2007年第1期28卷 28-35页

作者： Yan-fei WANG~2 Hong TIAN~2 Chao-shu TANG~(3,4) Hong-fang JIN~2 Jun-bao DU~(2,4,5)2 Department of Pediatrics,peking university first hospital,beijing 100034.china 3 institute of cardiovascular diseases,peking university first hospital,beijing 100034.china,4.key laboratory of molecular cardiovascular diseases,ministry of education,beijing 100034.china Department of Pediatrics Peking University First Hospital Beijing China institute of cardiovascular diseases Peking University First Hospital Beijing China key laboratory of molecular cardiovascular diseases Ministry of Education Beijing China

Aim:To explore the role of carbon monoxide(CO)in the regulation of hypoxicpulmonary artery smooth muscle cell(PASMC)proliferation and apoptosis bynitric oxide(NO).Methods:PASMC of Wistar rats was cultured in vitro in thepresence of a NO donor,sodium nitroprusside,or an inhibitor of heine oxygenase(HO),zinc protoporphyrin-IX,or under both normoxic and hypoxic *** and carboxyhemoglobin in PASMC medium were detected *** proliferating and apoptotic percentage of PASMC wasmeasured by flow *** expression of HO-1 mRNA in PASMC wasanalyzed by fluorescent real-time quantitative PCR,and the proliferating cell nuclearantigen and caspase-3 were examined by immunocytochemical ***:The results showed that hypoxia suppressed NO generation from PASMC,whichpromoted hypoxic PASMC proliferation and induced ***,hy-poxia induced HO-1 expression in PASMC and promoted CO production fromPASMC,which inhibited PASMC proliferation and regulated PASMC *** upregulated the expression of HO-1 mRNA in hypoxic PASMC;NO also inhib-ited proliferation and promoted apoptosis of hypoxic PASMC,possibly by regu-lating the production of ***:The results indicated that CO couldinhibit proliferation and regulate apoptosis of PASMC,and NO inhibited prolifera-tion and promoted apoptosis of hypoxic PASMC,possibly by regulating the pro-duction of CO.

关键词： hypoxia proliferation apoptosis carbon monoxide nitric oxide

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Sodium hydrosulfide alleviated pulmonary vascular structural remodeling induced by high pulmonary blood flow in rats

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Acta Pharmacologica Sinica 2006年第8期27卷 971-980页

作者： Xiao-hui LI~2 Jun-bao DU~(2,6) Ding-fang BU~3 Xiu-ying TANG~4 Chao-shu TANG~5 ~1Department of Pediatrics,peking university first hospital,key laboratory of molecular cardiovascular diseases,ministry of education ~3 laboratory Center ~4laboratory of Electron Microscopy,peking university first hospital,beijing 100034.china ~5Department of Physiology,peking university Health Science Center,beijing 100083,china Department of Pediatrics Peking University First Hospital Key Laboratory of Molecular Cardiovascular Diseases Ministry of Education Beijing China laboratory Center Peking University First Hospital Beijing China laboratory of Electron Microscopy Peking University First Hospital Beijing China Department of Physiology Peking University Health Science Center Beijing China

Aim:To explore the possible role of endogenous hydrogen sulfide （H2S）,a novelgasotransmitter,in the pathogenesis of pulmonary vascular structural remodeling（PVSR） induced by high pulmonary blood ***:Thirty-two Sprague-Dawley male rats were randomly divided into sham,shunt,sham+NaHS （a H2Sdonor） and shunt+NaHS *** in shunt and shunt+NaHS groups under-went an abdominal aorta-inferior vena cava shunt,and rats in shunt+NaHS andsham+NaHS groups were intraperitoneally injected with *** was inves-tigated using optical microscope and transmission electron *** H2S was evaluated by sulfide-sensitive *** oxide synthase（NOS）,heme oxygenase （HO-1）,proliferative cell nuclear antigen （PCNA） andextracellular signal-regulated kinase （ERK） activation were analyzed by ***:After 11 weeks of shunting,PVSR developed with a decrease inlung tissue H2S production and an increase in nitric oxide （NO）.However,lungtissue carbon monoxide （CO） did not *** the treatment with NaHS for11 weeks,H2S donor ameliorated PVSR and downregulated PCNA expression andERK activation with an increase in lung tissue CO production and HO-1 proteinexpression but a decrease in NO production,NOS activity and eNOS proteinexpression in shunted ***:H2S exerted a regulatory effect on PVSRinduced by high pulmonary blood ***,H2S down-regulated theERK/MAPK signal pathway,inhibited the NO/NOS pathway and enhanced theCO/HO pathway in rats with high pulmonary blood flow.

关键词： hydrogen sulfide pulmonary hypertension structure remodeling nitric oxide/nitric oxide synthase carbon monoxide/heme oxygenase

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Taurine inhibits ischemia/reperfusion-induced compartment syndrome in rabbits

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Acta Pharmacologica Sinica 2005年第7期26卷 821-827页

作者： Ji-xian WANG~(2,3) Yan LI~2 Li-ke ZHANG~4 Jing ZHAO~5 Yong-zheng PANG~(2,3) Chao-shu TANG~(3,5) Jing ZHANG~(2,3,6) 1 institute of cardiovascular Disease Research,The first hospital of peking university,beijing 100034.china 3 key laboratory of molecular cardiovascular Science,ministry of education,beijing 100083,china 4 Department of Pathophysiology,Capital institute of Medicine,beijing 100054,china 5 Department of Physiology Health Center of Medical Sciences,peking university,beijing 100083,china institute of cardiovascular Disease Research The First Hospital of Peking University Beijing China key laboratory of molecular cardiovascular Science Ministry of Education Beijing China Department of Pathophysiology Capital Institute of Medicine Beijing China Department of Physiology Health Center of Medical Sciences Peking University Beijing China

Aim:To investigate effects of taurine on ischemia/reperfusion(I/R)-induced com-partment syndrome in rabbit hind ***:Rabbits underwent femoralartery occlusion after ligation of branches from terminal aorta to femoral *** a 7-h ischemia,reperfusion was established with the use of heparinizedpolyethylene *** received taurine(1 g/kg)or normal saline(control)by iv infusion 10 min before shunt *** reperfusion,anterior com-partment pressure(ACP)was monitored continuously in the left lower *** muscle triphenyltetrazolium chloride(TTC)level,taurine contentand myeloperoxidase activity were *** stress was induced in thein vitro gastrocnemius muscle slices by free radical generating systems(FRGS),and the malondialdehyde content was measured in presence or absence of ***:After 7 h of ischemia,none of the parameters that we measured weredifferent from those before ischemia,except that TTC reduction decreased by80%.In the control group,after 2 h of reperfusion,ACP increased 4.5-fold,andgastrocnemius muscle taurine content was reduced by 33%.In taurine-treatedanimals,at 2 h reperfusion,the mean arterial blood pressure and heart rate wereincreased,by 6% and 10%.ACP decreased by 39%,muscle edema decreased by16%,TTC reduction increased by 150%,and lactate dehydrogenase decreased by36% compared to control *** and muscle taurine content increased by70% and 88%,*** the taurine-treated group,at 2 h repeffusion,plasmamalondialdehyde and conjugated diene content were decreased by 38% and 23%,respectively,and muscle malondialdehyde and conjugated diene content decreasedby 22% and 30%,respectively compared to the control *** 2 h reperfusion,myeloperoxidase activity was increased 3.5-fold in control *** the in vitrostudy,taurine decreased malondialdehyde content in muscle slices incubatedwith hypochlorous acid in a dose-dependent manner,but there was no changewhen incubated

关键词： taurine compartment syndromes reperfu sion injury

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Hydrogen sulfide ameliorates vascular calcification induced by vitamin D3 plus nicotine in rats

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Acta Pharmacologica Sinica 2006年第3期27卷 299-306页

作者： Sheng-ying WU~(2,6) Chun-shui PAN~3 Bin GENG~3 Jing ZHAO~3 Fang YU~3 Yong-zheng PANG~3 Chao-shu TANG~4 Yong-fen QI~(3,4,5) ~2institute of cardiovascular Disease,peking university first hospital.beijing 100034 ~3Department of Physiology and Pathophysiology,peking university Health Science Center,beijing 100083,china,~4key laboratory of molecular cardiovascular Science,ministry of education,beijing 100083,china institute of cardiovascular Disease Peking University First Hospital Beijing China Department of Physiology and Pathophysiology Peking University Health Science Center Beijing China key laboratory of molecular cardiovascular Science Ministry of Education Beijing China

Aim:To investigate the role of the endogenous cystathionine γ-synthase(CSE)/hydrogen sulfide(H2S)pathway in vascular calcification in ***:A ratvascular calcification model was established by administration of vitamin D3 plusnicotine(VDN).The amount of CSE and osteopontin(OPN)mRNA was deter-mined by using semi-quantitative reverse-transcription polymerase chain *** calcium content,45Ca2+accumulation and alkaline phosphatase(ALP)activitywere measured.H,S production and CSE activity were ***:yonKossa staining produced strong positive black/brown staining in areas amongthe elastic fibers of the medial layer in the calcified *** calcium content,45Ca2+accumulation and ALP activity in calcified arteries increased by 6.77-,1.42-,and 1.87-fold,respectively,compared with *** expression of the OPNgene was upregulated(P45Ca2+uptake and ALP activity in the VDN plus NaHSgroup was lower than that in the VDN *** content of calcium and45Ca2+accumulation and activity of ALP in the aorta were 34.8%,40.75% and 63.5% lowerin the low-dosage NariS group than in the VDN group,respectively(P45Ca2+and activity of ALP was 83.9%,37.8 % and 46.2% lower in the aorta in the high-dosage NariS group than in theVDN group,respectively(P<0.01).The expression of the OPN gene ***:The production of H,S,and CSE activity were de-creased and CSE gene expression was downregulated in rats with vascularcalcification.H2S can ameliorate vascular calcification,suggesting that the H2S/CSE pathway plays a regulatory role in the pathogenesis of vascular calcification.

关键词： hydrogen sulfide cystathionine-lyase vascular calcification mRNA

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Chinese consensus on the diagnosis and treatment of immunoglobulin light-chain cardiac amyloidosis

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Chinese Medical Journal 2024年第2期137卷 127-129页

作者： Kaini Shen Zhuang Tian Yajuan Gao Yining Wang Li Huo Jian Li Yun Zhang Shuyang Zhang On behalf of Chinese Society of Rare diseases and Rare diseases Branch of china Research hospital Association Department of Hematology State Key Laboratory of Complex Severe and Rare DiseasesPeking Union Medical College HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100730China Department of Cardiology State Key Laboratory of Complex Severe and Rare DiseasesPeking Union Medical College HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100730China Department of Clinical Medicine Chinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100730China Department of Radiology State Key Laboratory of Complex Severe and Rare DiseasesPeking Union Medical College HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100730China Department of Nuclear Medicine Beijing Key Laboratory of Molecular Targeted Diagnosis and Therapy in Nuclear MedicineState Key Laboratory of Complex Severe and Rare DiseasesCenter for Rare Diseases ResearchPeking Union Medical College HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100730China Department of Cardiology The Key Laboratory of Cardiovascular Remodeling and Function ResearchChinese Ministry of EducationChinese National Health Commission and Chinese Academy of Medical SciencesThe State and Shandong Province Joint Key Laboratory of Translational Cardiovascular MedicineQilu HospitalCheeloo College of MedicineShandong UniversityJinanShandong 250012China cardiovascular Disease Research Center of Shandong first Medical university Central Hospital Affiliated to Shandong First Medical UniversityJinanShandong 250013China 不详

Epidemiology of Amyloid Light-Chain Cardiac Amyloidosis(AL-CA)The annual incidence of amyloid light-chain(AL)amyloidosis is 3-5/million,and the incidence in men is slightly higher than that in ***,70%of patients with ... 详细信息

关键词： amyloid cardiac diagnosis

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Cardioprotective effects of ghrelin and des-octanoyl ghrelin on myocardial injury induced by isoproterenol in rats

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Acta Pharmacologica Sinica 2006年第5期27卷 527-535页

作者： LLian LI~2 Li-ke ZHANG~5 Yong-zheng PANG~(2.4) Chun-shui PAN~(3.4) Yong-fen QI~(3.4) Li CHEN~4 Xian WANG~(3,4) Chao-shu TANG~(3,4) Jing ZHANG~(2,4,6) ~2institute of cardiovascular Research,peking university first hospital,beijing 100034.china:~3Department of Physiology and Pathophysiology,peking university Health Science Center,beijing 100083,china ~4key laboratory of the ministry of education on molecular Cardiology,beijing 100083,china:~5Department of Pathophysiology,Capital university of Medicine,beijing 100054,china institute of cardiovascular Research Peking University First Hospital Beijing China Department of Pathophysiology Capital University of Medicine Beijing China key laboratory of the ministry of education on molecular Cardiology Beijing China Department of Physiology and Pathophysiology Peking University Health Science Center Beijing China

Aim:To determine the cardioprotective action of ghrelin and des-octanoyl ghrelinin rats with isoproterenol-induced myocardial ***:Rats were subcu-taneously injected with isoproterenol （ISO;20,10,and 5 mg/kg） on d 1,2 and 3,respectively,and then 3 mg/kg for the next 7d with or without ghrelin or des-octanoyl-ghrelin （100μg/kg,twice daily）.Plasma ghrelin and growth hormonelevels were assayed using radioimmunoassay *** hormone secreta-gogue receptor （GHSR） and ghrelin mRNA were determined using *** binding capacity and the affinity for [3H]ghrelin were determined by re-ceptor binding ***:Compared with controls,ISO-treated rats showedsevere myocardial injury,cardiomegaly,infarction-like necrosis and massive fi-brosis with increases in irradiated-ghrelin （ir-ghrelin） content in plasma by 67%and myocardia by 66% and in the mRNA level in the myocardia by 93% （P3H]ghrelin for myocardial sarcolemma was higherin ISO-treated rats than in *** administration improved cardiac func-tion and ameliorated cardiomegaly and attenuated myocardial lipid peroxidationinjury and relieved cardiac fibrosis as compared with ISO treatment ***-istration of des-octanoyl ghrelin effectively antagonized ISO-induced myocardialinjury and improved all parameters ***,the therapeutic effect ofdes-octanoyl ghrelin was significantly weaker than that of *** plasmagrowth hormone level increased markedly,by 1.5-fold （P<0.01）,with ghrelinadministration as compared with that in controls,but was unaltered in the des-octanoyl ghrelin ***:Myocardial ghrelin and GHSR were up-regulated during ISO-induced myocardial *** protective effect of ghrelinagainst ISO-induced cardiac function injury and fibrosis was more potent thanthat of des-octanoyl ghrelin,which suggests that ghrelin could be an endog

关键词： ghrelin des-octanoyl ghrelin myocardium fibrosis isoproterenol

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Crosstalk between signaling pathways of adrenoreceptors and signal transducers and activators of transcription 3(STAT3)in heart

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Acta Pharmacologica Sinica 2007年第2期28卷 153-161+163-165页

作者： Kai-zheng GONG Hui ZHANG Jian-hai DU You-yi ZHANG~2 institute of Vascular Medicine,peking university Third hospital,key laboratory of molecular cardiovascular Sciences,ministry of education beijing 100083,china institute of Vascular Medicine Peking University Third Hospital Key Laboratory of Molecular Cardiovascular Sciences Ministry of Education Beijing China

Recently,there have been important advancements in our understanding of thesignaling mechanisms of adrenoreceptors(AR)and signal transducers and acti-vators of transcription 3(STAT3).While their crucial roles in the pathologicalprocesses of the heart are well established,accumulating evidence suggests thereis a complex pattern of crosstalk between these 2 signaling ***,the potential for crosstalk occurs at multiple levels in each signaling cascade andinvolves receptor transactivation,G proteins,small GTPases,cyclic adenosine 3’,5’-monophosphate/protein kinase A,protein kinase C,scaffold/adaptor proteins,protein tyrosine kinases,and mitogen-activated protein *** addition,post-translational modification(eg acetylation)of STAT3 may provide a link betweenSTAT3 and AR *** particular,crosstalk between these 2 systems in theheart would appear to be dependent upon the species/tissue studied,develop-mental stage,and eliciting *** at least partly accounts for the epige-netic effects on biological function that is mediated by the 2 signaling *** of these mechanisms will provide new targets in the development ofnovel clinical strategies for heart disorders.

关键词： receptors adrenergic signal transduction STAT3 transcription factor heart

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AICAR inhibits proliferation and induced S-phase arrest,and promotes apoptosis in CaSki cells

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Acta Pharmacologica Sinica 2007年第12期28卷 1984-1990页

作者： Tong-ju GUAN~2,Feng-jin QIN~3,Jian-hai DU~4,Li Geng~3,You-yi ZHANG~(4,5),Min LI~(2,5)~2 institute of Pathology,The School of Basic Medicine,Lanzhou university,Lanzhou 730000,china ~3 Department of Gynaecology andObstetrics,peking university Third hospital,beijing 100083,china ~4 institute of Vascular Medicine,peking university Third hospital andkey laboratory of molecular cardiovascular Sciences ministry of education,beijing 100083,china institute of Pathology The School of Basic Medicine Lanzhou University Lanzhou China Department of Gynaecology and Obstetrics Peking University Third Hospital Beijing China institute of Vascular Medicine Peking University Third Hospital and Key Laboratory of Molecular Cardiovascular Sciences Ministry of Education Beijing China

Aim:The aim of the present study was to determine the effect of 5-aminoimidazole-4-carboxamide-ribonucleoside （AICAR） on proliferation,cell cycle,and apoptosisin the human epithelial cervical cancer cell line CaSki ***:Cell countand 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide assay were usedto determine cell proliferation and *** 33258 staining was con-ducted to distinguish the apoptotic *** cycle and Annexin-V/propidiumiodide staining were analyzed by fluorescence-activated cell sorting （FACS）.AWestern blot assay was used to evaluate the expression of AKT （also known asprotein kinase B）,mammalian target of rapamycin （mTOR）,p53,and extracellularsignal-regulated kinase （ERK）.Results:AICAR （500 μmol/L） significantly inhibi-ted the proliferation of CaSki cells treated for 24,48,and 72 h as determined by *** cells at the G1and G2phases were dramatically decreased while cells atthe S phase were increased in response to AICAR treatment for 24,48,and 72 *** MTT assay showed less viable cells and Hoechst fluorescent staining showedmore apoptotic cells upon AICAR *** results of the Annexin-Vstaining demonstrated a time-dependent increase of apoptosis in cells treatedwith AICAR for 24,36,and 48 ***,AICAR activated caspase-3 in atime-dependent *** was also found that AICAR inhibited the phosphory-lation of AKT and mTOR,which are important kinases regulating cell growth *** stimulation obviously increased the expression of the tumorsuppressor p53 and the phosphorylation of ***:AICAR inhibitedproliferation and induced S phase arrest and promoted apoptosis in CaSki cells,which might be mediated by the downregulation of the AKT/mTOR pathway andthe upregulation of the p53/ERK pathway.

关键词： AICAR proliferation apoptosis CaSki cells

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Overexpression of heat-shock protein 20 in rat heart myogenic cells confers protection against simulated ischemia/reperfusion injury

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Acta Pharmacologica Sinica 2005年第9期26卷 1076-1080页

作者： Yan-hui ZHU Xian WANG~2 Department of Physiology and Pathophysiology,Basic Medical College,key laboratory of molecular cardiovascular Biology,ministry of education,peking university,beijing 100083,china Department of Physiology and Pathophysiology Basic Medical College Key Laboratory of Molecular Cardiovascular Biology Ministry of Education Peking University Beijing China

Aim:To explore whether overexpression of the small heat shock protein HSP20 inrat cardiomyocytes protects against simulated ischemia/reperfusion(SI/R)***:Recombinant adenovirus expressing HSP20 was used to infect rat H9c2cardiomyocytes at high efficiency,as assessed by green fluorescent protein.H9c2cells were subjected to SI/R stress;survival was estimated through assessment oflactate dehydrogenase and cell apoptosis through caspase-3 ***:Overexpression of HSP20 decreased lactate dehydrogenase release by 21.5% andcaspase-3 activity by 58.8%.Pretreatment with the protein kinase C inhibitor Ro-31-8220(0.1 μmol/L)for 30 min before SI/R canceled the protective effect of *** selective mitochondrial K+awP channel inhibitor 5-hydroxydecanoate(100 μmol/L)had a similar ***,the non-selective K~+ATPchannel inhibitorglibenclamide(100 μmol/L)had no significant ***:These dataindicate that the protective effect of HSP20 in vitro is primarily due to reducednecrotic and apoptotic death of cardiomyocytes,possibly via the protein kinaseC/mitochondrial K~+ATP pathway.

关键词： reperfusion injury adenovirus apoptosis necrosis heat-shock proteins

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Calcitonin gene-related peptide inhibits interleukin-1β-induced interleukin-8 secretion in human type Ⅱ alveolar epithelial cells

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Acta Pharmacologica Sinica 2006年第10期27卷 1340-1345页

作者： Wen-jing LI Teng-ke WANG Xian WANG~2 Department of Physiology,School of Basic Medical Sciences,peking university,key laboratory of molecular cardiovascular Science,ministry of education,beijing 100083,china Department of Physiology School of Basic Medical Sciences Peking University Key Laboratory of Molecular Cardiovascular Science Ministry of Education Beijing China

Aim:Our previous data have shown that type Ⅱ alveolar epithelial(AEⅡ)cellsexpress neuropeptide calcitonin gene-related peptide(CGRP),and that pro-in-flammatory factor interleukin 1-β(IL-1β)induces CGRP secretion in the A549 hu-man AEⅡ cell *** the present study,we investigated the effect of endogenousand exogenous CGRP on IL-1β-induced chemokine interleukin-8(IL-8)***:We used enzyme-linked immunosorbent assay(ELISA)and RT-PCR todetect IL-8 protein and mRNA levels,respectively,siRNA and the stably trans-fected cell line were used to knock down and overexpress the CGRP gene,respectively,and chemiluminescence assay was used to detect reactive oxygenspecies(ROS)***:CGRP-1 receptor antagonist hCGRP8-37(0.1-1nmol·L-1)greatly amplified IL-1β-induced IL-8 *** inhibition of CGRPexpression by siRNA significantly increased IL-8 secretion upon IL-1β ***,cell clones stably transfected with CGRP showed significantly inhibitedmRNA and protein levels of IL-8 induced by 1L-1β.Conclusion:These data implythat AEⅡ cell-derived CGRP suppress IL-1β-induced IL-8 secretion in an autocrine/paracrine *** investigation showed that CGRP attenuated IL-1β-arousedROS formation,which is an early indication of pro-inflammatory factor signaling.

关键词： type Ⅱ alveolar epithelial cells interleukinl interleukin-8 calcitonin gene-related peptide anti-inflammation lung reactive oxygen species

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