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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 ~4.aboratory of electron microscopy,peking university first hospital,Beijing 10003.,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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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 10003.,china 3 Institute of Cardiovascular Diseases,peking university first hospital,Beijing 10003.,china,4.Key Laboratory of Molecular Cardiovascular Diseases,Ministry of Education,Beijing 10003.,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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Urotensin Ⅱ accelerates cardiac fibrosis and hypertrophy of rats induced by isoproterenol

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Acta Pharmacologica Sinica 2007年第1期28卷 36-43页

作者： Yong-gang ZHANG~(2,5) Yu-guang LI~2 Bao-guo LIU~3 Rui-hong WEI~2 Dong-ming WANG~2 Xue-rui TAN~2 Ding-fang BU~4.Yong-zheng PANG~4.Chao-shu TANG~4. Department of Cardiovascular Diseases,first Affiliated hospital,Shantou university Medical College,Shantou 51504.,china 3 The Affiliated hospital,Medical School of Hebei university of Engineering,Hebei 056029,china,4.Institute of Cardiovascular Research,peking university first hospital,Beijing 10003.,china Department of Cardiovascular Diseases First Affiliated Hospital Shantou University Medical College Shantou China The Affiliated hospital Medical School of Hebei University of Engineering Hebei China Institute of Cardiovascular Research Peking University First Hospital Beijing China

Aim:To study whether urotensin II（UII）,a potent vasoconstrictive peptide,isinvolved in the development of cardiac hypertrophy and fibrogenesis of ratsinduced by isoproterenol（ISO）.Methods:Thirty male Wistar rats were randomlydivided into 3 *** 1 was the healthy control group,group 2 was the ISOgroup,and group 3 was the ISO+UII *** groups 2 and 3,ISO(5 mg-kg-1.d-1)wasgiven（sc）once daily for 7 *** 3 was also given UII in the first day [3 nmol/kg（5μg/kg）,iv],followed by sc（1.5 μg/kg）twice *** 1 received 0.9% *** receptor（UT）mRNA expression was determined by *** contents ofUII and angiotensin II（Ang II）were determined by *** vitro,the effects of UII on DNA/collagen synthesis of cardiac fibroblasts were deter-mined by [3H]thymidine/[3H]proline ***:The ratio of heartweight/body weight,plasma lactate dehydrogenase activity,myocardialmalondialdehyde and hydroxyproline concentration increased significantly in theISO group,as well as UT mRNA expression,plasma and cardiac UII and ventricu-lar Ang II,compared with the control group（P<0.01）.ISO induced significantmyocardial ***,UII+ISO co-treatment significantly increasedthe changes of biochemical markers of injury and the degree of cardiac hypertro-phy and *** vitro,5×10～9-5×10-7mol/L UII stimulated[3H]thymidine/[3H]proline incorporation into cardiac fibroblasts in a dose-dependent manner（P<0.01）.Conclusion:These results suggest that UII was involved in the development ofcardiac fibrosis and hypertrophy by synergistic effects with ISO.

关键词： cardiac remodeling cardiac fibrosis GPR14.receptor urotensin II collagen

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Interaction between hydrogen sulfide/cystathionine γ-lyase and carbon monoxide/heme oxygenase pathways in aortic smooth muscle cells

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Acta Pharmacologica Sinica 2006年第12期27卷 1561-1566页

作者： Hong-fang JIN~2 Jun-bao DU~(2,4.Xiao-hui LI~2 Yan-fei WANG~2 Yin-fang LIANG~2 Chao-shu TANG~3 2 Department of Pediatrics,peking university first hospital,Beijing 10003.,china 3 Institute of Cardiovascular Research,peking university first hospital,Beijing 10003.,china Department of Pediatrics Peking University First Hospital Beijing China Institute of Cardiovascular Research Peking University First Hospital Beijing China

Aim:To investigate the interaction between hydrogen sulfide（H2S）/cystathion-ine γ-lyase（CSE）and carbon monoxide（CO）/heme oxygenase（HO）pathways inaortic smooth muscle cells（ASMC）.Methods:The ASMCs were divided into thefollowing groups:（1）the control group;（2）the zinc protoporphyrin（ZnPP）20μmol/L group;（3）the propargylglycine（PPG）2 mmol/L,4.mmol/L and 10 mmol/Lgroups;and（4.the sodium hydrosulfide（NariS）1×10-5mol/L,1×10-4.ol/L and1×10-3mol/L *** of the groups was further divided into 6h,12h,18hand 24. *** CO level,represented by carboxyhemoglobin（HbCO）content was measured using a spectrophotometric method and H2S content wasdetected by a sensitive electrode *** and HO-1 expressions were de-tected by Western ***:The H2S content in the medium and CSEexpression by ASMC were markedly increased by ZnPP compared with the con-trol *** content in the medium and HO-1 expression by the ASMCstarted strengthening following 24. treatment with PPG at 2 mmol/L,but werefurther strengthened following 18h and 24. treatment with PPG at 4.mmol/Lcompared with the controls（P4.ol/Ldecreased the HbCO level in the medium and HO-1 expression by the ASMC after6h and 12h treatment,while NariS at 1×10-3mol/L decreased them at all timepoints of the ***:The results suggested that endogenousCO/HO and H2S/CSE pathways inhibited each other in ASMC under physiologi-cal conditions.

关键词： hydrogen sulfide cystathionine γ-lyase carbon monoxide heme oxygenase

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Deficit of mitochondria-derived ATP during oxidative stress impairs mouse MII oocyte spindles

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Cell Research 2006年第10期16卷 841-850页

作者： Xiao Zhang~(1,2,*) Xue Qing Wu~(1,3,*) Shuang Lu~(4.5,6) Ying Lu Guo~1 Xu Ma~(4.5,6) ~1peking university first hospital,Institute of Urology of peking university,Beijing 10003.,{4. ~2Reproductive and Genetic Center of peking university first hospital,Beijing 10003.,{4. ~3Department of Obstetrics and Gynecology,Shanxi Medical university Second hospital,Taiyuan 030000,{4. ~4.eproductive and Genetic Center of National Research Institute for Family Planning,Beijing 10003.,{4. ~5Department of Genetics, peking Union Medical College, Beijing 10003.. {4. ~6 WHO Collaborative Center for Research in Human Reproduction,Beijing 10003.,{4. peking university first hospital Institute of Urology of Peking University Beijing China Reproductive and Genetic Center of peking university first hospital Beijing China Department of Obstetrics and Gynecology Shanxi Medical University Second Hospital Taiyuan China Reproductive and Genetic Center of National Research Institute for Family Planning Beijing China Department of Genetics Peking Union Medical College Beijing China WHO Collaborative Center for Research in Human Reproduction Beijing China

Although the role of oxidative stress in maternal aging and infertility has been suggested,the underlying mechanismsare not fully *** present study is designed to determine the relationship between mitochondrial functionand spindle stability in metaphase Ⅱ （MⅡ） oocytes under oxidative stress.MⅡ mouse oocytes were treated with H2O2inthe presence or absence of permeability transition pores （PTPs） blockers cyclosporin A （CsA）.In addition,antioxidantN-acetylcysteine （NAC）,F0/F1synthase inhibitor oligomycin A,the mitochondria uncoupler carbonyl cyanide 4.trifluoro-methoxyphenylhydrazone （FCCP） or thapsigargin plus 2.5 mM Ca2+(Th+2.5 mM Ca2+) were used in mechanistic *** analyses ofoocyte spindles and chromosomes were performed and mitochondrial membrane potential（Δψm）,cytoplasmic tree calcium concentration ([Ca2+]c) and cytoplasmic ATP content within oocytes were also *** a time- and H2O2dose-dependent manner,disruption of meiotic spindles was found after oocytes were treated withH2O2,which was prevented by pre-treatment with *** of H2O2led to a dissipation of Δψm,an increasein [Ca2+]cand a decrease in cytoplasmic ATP *** detrimental responses of oocytes to H20,treatment could beblocked by pre-incubation with *** to H2O2,both oligomycin A and FCCP dissipated Δψm,decreased cytoplas-mic ATP contents and disassembled MⅡ oocyte spindles,while high [Ca2+]calone had no effects on spindle *** conclusion,the decrease in mitochondria-derived ATP during oxidative stress may cause a disassembly of mouse MⅡoocyte spindles,presumably due to the opening of the mitochondrial PTPs.

关键词： spindle oxidative stress mitochondria permeability transition pore ATP

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Mycophenolic acid inhibits SLE-associated cytokine expression and promotes apoptosis of peripheral blood mononuclear cells from patients with systemic lupus erythematosus

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Acta Pharmacologica Sinica 2006年第8期27卷 1051-1057页

作者： Ding-lei SU~(2,3) Hui-juan WANG~2 Xiao-hui JI~(2,5) Yuan-yuan LI~4.Heng-bao XUAN~4.Chun HENG~4.Yu-feng LI~4.~2Department of Immunology,Nanjing Medical university,Nanjing 210029,china:~3Department of Hematology,Nanjing first hospital Affiliated to Nanjing Medical university,Nanjing 210029,china ~4.epartment of Hematology,Affiliated Huai'an first hospital of Nanjing Medical university,Huai'an 223300.china Department of Immunology Nanjing Medical University Nanjing China Department of Hematology Nanjing First Hospital Affiliated to Nanjing Medical University Nanjing China Department of Hematology Affiliated Huai'an First Hospital of Nanjing Medical University Huai'an China

Aim:To investigate the effect of the novel immunosuppressant mycophenolicacid（MPA）on cytokine production and apoptosis of the peripheral blood mono-nuclear cells（PBMC）of patients with systemic lupus erythematosus（SLE）.Methods:The levels of IL-10,IL-12,IFN-γ,sFas and sFasL in the supernatants ofcultured PBMC from 4. SLE patients was determined by the ABC-ELISA *** percentage of IFN-γIL- 10-,IFN-γ-IL-10+,and IFN-γ+IL-10+subsets in CD4.ceils were detected by three-color flow *** percentage of apoptoticTh cells was detected by AV-FITC/PI flow *** from 22 sex-andage-comparable healthy people were used as normal ***:The lev-els of IL-10,IL-12,and IFN-γwere all significantly elevated in the supernatants ofcultured PBMC from SLE samples,compared with normal *** enhancedproductions of IL-10,IL-12,and IFN-γ by PBMC from SLE both spontaneouslyand stimulated by phytohaemagglutinin（PHA）were significantly reduced by *** percentages of CD4.IFN-γIL-10+and CD4.IFN-γ+IL-10+cell subsets in cul-tured PBMC from SLE were significantly increased,but decreased when MPA wasadded into the *** being cultured in vitro for 4.h,the PBMC of SLEpatients showed a higher secretion of sFasL as well as a higher percentage *** significantly increased the apoptotic percentage of SLE PBMC,but reduced the secretion of sFasL and ***:MPA reduces theabnormal production of SLE-associated cytokines,such as IL-10,IL-12,and IFN-γ,inhibits the increase of CD4.IFN-γ+IL-10,CD4.IFN-γIL-10+and CD4.IFN-γ+IL-10+subset;and promotes the apoptosis of PBMC in SLE patients,which may beassociated with the therapeutic mechanism of MPA for SLE.

关键词： systemic lupus erythematosus mycophenolic acid cytokine apoptosis therapeutic mechanism

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Microtubule stability and MAP1B upregulation control neuritogenesis in CAD cells

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Acta Pharmacologica Sinica 2006年第9期27卷 1119-1126页

作者： Wen LI~(2,5)Jin-tang XIA~3 Yue FENG~(4.5)2 Laboratory of Surgery,The first Affiliated hospital,Sun Yat-sen university,Guangzhou 510080,{4. 3 Department of General Surgery,The first People's hospital of Guangzhou,Guangzhou 510180,{4. 4.Department of Pharmacology,Emory university School of Medicine,USA Laboratory of Surgery The First Affiliated Hospital Sun Yat-sen University Guangzhou China Department of General Surgery The First People's Hospital of Guangzhou Guangzhou China Department of Pharmacology Emory University School of Medicine USA

Aim:To study the role of microtubule dynamics and microtubule associated pro-tein 1B(MAP1B)in regulation of the neurite extension in CAD catecholaminergicneuronal cell ***:The neuritogenesis of the CAD cells was abolishedby inhibiting microtubule polymerization with nocodazole and by blocking micro-tubule depolymerization with ***1B and tubulin protein expression wasdetected by Western *** staining of tubulins was observedby fluorescent and confocal ***:Microtubule dynamics wasessential for CAD neurite *** analysis revealed that neurite exten-sion was much more sensitive to nocodazole than to taxol,suggesting a func-tional requirement for highly active microtubule assembly.A remarkableupregulation of MAP IB protein was detected during neurite extension accompa-nied with increased microtubule ***:Upregulation of MAP1Bleads to the stabilization of newly formed microtubules in the developing neurites,which in turn promotes neurite extension.

关键词： microtubule stability microtubule associated protein 1B neuritogenesis

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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 {4.,Beijing 100083,china ~4.Institute of Vascular Medicine,peking university Third {4. 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 24.4.,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 24.4.,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 4. ***,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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Atomic Force microscopy-based Cell Nanostructure for Ligand-conjugated Quantum Dot Endocytosis

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Acta Biochimica et Biophysica Sinica 2006年第9期38卷 646-652页

作者： Yun-Long PAN~1* Ji-Ye CAI~2 Li QIN~3 Hao WANG~4. 1 The first Affiliated hospital of Jinan university,Guangzhou 510632,china 2 College of Life Science and Technology,Jinan university,Guangzhou 510632,china 3 Department of Histology and Embryology,Medical College of Jinan university,Guangzhou 510632,china 4.Information and Optoelectronic Science and Engineering.South china Normal university,Guangzhou 510631,china The first Affiliated hospital of Jinan universityGuangzhou 510632 China College of Life Science and Technology Jinan UniversityGuangzhou 510632 China Department of Histology and Embryology Medical College of Jinan UniversityGuangzhou 510632 China School for Information and Optoelectronic Science and Engineering South China Normal UniversityGuangzhou 510631 China

While it has been well demonstrated that quantum dots (QDs) play an important role inbiological labeling both in vitro and in vivo,there is no report describing the cellular nanostructure basis ofreceptor-mediated ***,nanostructure evolution responses to the endocytosis of transferrin(Tf)-conjugated QDs were characterized by atomic force microscopy (AFM).AFM-based nanostructureanalysis demonstrated that the Tf-conjugated QDs were specifically and tightly bound to the cell receptorsand the nanostructure evolution is highly correlated with the cell membrane receptor-mediated ***,confocal microscopic and flow cytometry results have demonstrated the specificity anddynamic property of Tf-QD binding and *** found that the internalization of Tf-QD is linearlyrelated to ***,while the nanoparticles on the cell membrane increased,the endocytosis was stillvery active,suggesting that QD nanoparticles did not interfere sterically with the binding and function ***,ligand-conjugated QDs are potentially useful in biological labeling of cells at a nanometerscale.

关键词： quantum dot endocytosis nanostructure atomic force microscopy

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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 10003.,china:~3Department of Physiology and Pathophysiology,peking {4. Health Science Center,Beijing 100083,china ~4.ey Laboratory of the Ministry of Education on Molecular Cardiology,Beijing 100083,china:~5Department of Pathophysiology,Capital {4. 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% （P<0.01）.ISO-treated rats had 95% （P<0.01） higher GHSR mRNA levels in the *** maximal binding capacity of [3H]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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