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Taurine inhibits ischemia/reperfusion-induced compartment syndrome in rabbits

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 10003.,China 3.Key Laboratory of Molecular Cardiovascular Science,Ministry of Education,beijing 100083,China 4 {3. 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 3.%.In taurine-treatedanimals,at 2 h reperfusion,the mean arterial blood pressure and heart rate wereincreased,by 6% and 10%.ACP decreased by 3.%,muscle edema decreased by16%,TTC reduction increased by 150%,and lactate dehydrogenase decreased by3.% 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 3.% and 23.,respectively,and muscle malondialdehyde and conjugated diene content decreasedby 22% and 3.%,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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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 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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Taurine antagonized oxidative stress injury induced by homocysteine in rat vascular smooth muscle cells

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Acta Pharmacologica Sinica 2004年第3期25卷 87-92页

作者： Lin CHANG2,3.Jian-xin XU4,Jing ZHAO5,Yong-zheng PANG2,3.Chao-shu TANG2,3.Yong-fen QI5,6 2Institute of Cardiovascular Diseases,the FirstHospital,peking university,beijing 10003. 3.nstitute of Cardiovascular Diseases,peking university,{3. 4Instituteof Biophysics,Chinese Academy of sciences,beijing 100101 5department of physiology,health Science center,peking university,{3.,China Institute of Cardiovascular Diseases the First Hospital Peking University 北京 100034 Institute of Biophysics Chinese Academy of Sciences 北京 100101 department of physiology Health Science Center Peking University 北京 100083

AIM: To observe protective effects of taurine on reactive oxygen species generation induced by homocysteine in rat vascular smooth muscle cells (VSMC). METHODS: Rat VSMC was incubated with various concentrations of homocysteine and taurine. The lactate dehydrogenase (LDH) activity which released into culture medium was elevated as an indicator for VSMC injury. The reactive oxygen species (ROS) — hydrogen peroxide (H2O2) and superoxide anion (O2ˉ· )were measured with luminol or lucigenin chemiluminescences method, and the mitochondria Mn-superoxide dismutase (Mn-SOD) and catalase (CAT) were also measured in treated VSMC. RESULTS: LDH leakage from cultured VSMC treated with homocystenie, was increased (P5, 10, and 20 mmol/L) significantly antago- nized 0.5 mmol/L homocysteine-induced H2O2generation in VSMC in a concentration dependent manner (P0.05 vs control). In this study, the superoxide anion in VSMC was not detectable by chemiluminent method. In addition, treatment of VSMC with taurine increased mitochondria Mn-SOD and CAT activity in a concentration dependent manner (P5), but homocysteine decreased mitochondria Mn-SOD and CAT activity (P<0.01 vs control). In addition, co-administration of taurine markedly ameliorated homocysteine-induced inhibition of Mn-SOD and CAT activity in VSMC (P<0.01 vs homocysteine alone group). CONCLUSION: Taurine antagonized the effects of homocysteine on ROS generation and anti-oxidant enzyme activities in rat VSMC in vitro.

关键词： homocysteine taurine vascular smooth muscle mitochondria reactive oxygen species

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p3. MAPK mediates cardiovascular and behavioral responses induced by central IL-1β and footshock in conscious rats

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Acta Pharmacologica Sinica 2004年第3期25卷 12-16页

作者： Rui-mao ZHENG,Chang-jiang ZOU,Shi-gong ZHU2 department of physiology and Pathophysiology,{3. Science center,peking university,beijing 100083,China department of physiology and Pathophysiology Health Science Center Peking University 北京 100083

AIM: To investigate the roles of p3. mitogen-activated protein kinase (p3. MAPK) in the cardiovascular and behavioral responses induced by intracerebral ventricular injection (icv) of interleukin-1β (IL-1β) or footshock. METHODS: We examined the effects of p3. MAPK on mean artery blood pressure (mABP), heart rate (HR), and motor activity (MA) during central administration of IL-1β, or footshock after icv SB203.80 (a specific inhibitor of the p3. MAPK) with Cardiovascular and Behavior Telemetry System in conscious SD rats. RESULTS: (1) IL-1β (icv) or footshock remarkably rise the mABP, and the maximal changes are (7.8±1.8) and (12.3.3.5) mmHg, respectively, which was abrogated by the pretreatment with p3. inhibitor SB203.80 intracerebroventricularly. (2) Compared with icv saline group, the motor activity was significantly decreased in SB203.80 group with maximal changes (-7.6±1.1) counts/min after footshock. CONCLUSION: p3. MAPK plays an important role in the pres- sor response induced by central administration of IL-1β or footshock and change of motor activity after footshock in conscious rats.

关键词： mitogen-activated protein kinase p3. interleukin-1 blood pressure motor activity

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Effects of Ganoderma lucidum polysaccharides on proliferation and cytotoxicity of cytokine-induced killer cells

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Acta Pharmacologica Sinica 2005年第9期26卷 1130-1137页

作者： Xiao-ling ZHU Zhi-bin LIN department of Pharmacology,School of Basic medical Science,peking university {3. Science center,beijing 100083,China department of Pharmacology School of Basic Medical Science Peking University Health Science Center Beijing 100083 China

Aim:To study the effects(and the mechanisms thereof)of Ganoderma lucidumpolysaccharides(G/-PS)on the proliferation and the anti-tumor activity of cytokine-induced killer(CIK)cells,and to make use of CIK cells as a means to investigatethe interactions between Gl-PS and ***:CIK cells were preparedby using the standard protocol as a positive *** groups alsounderwent the standard protocol,except that Gl-PS(400 mg/L or 100 mg/L)wasadded and the dose of anti-CD3.and interleukin-2 they received was reduced by50% and 75%,*** negative controls,Gl-PS in the experimentalprotocol was replaced with soluble starch or methylcellulose(400 mg/L or 100 mg/L).CIK cell proliferation,cytotoxicity,and phenotype were determined by using theTrypan blue exclusion method,MTT assay,and flow ***:Bysynergizing cytokines,Gl-PS(400 mg/L or 100 mg/L)could decrease the amountof cytokine in lymphokine activated killer(LAK)cells and CIK cells culture,buthad no significant effect on the proliferation,cytotoxicity,or phenotype of LAKcells,or CIK cells induced by cytokines at higher doses alone,in which CIK cellsexpanded about 80-fold and the main effectors,CD3.+NK1.1~+ cells,expanded bymore than 15%.The cytotoxicity of CIK cells in experimental groups was 79.3.±4.7%,76.9%±6.8% versus the positive control 80.7%±6.8% against P815(P>0.05)and 88,9%±5.5%,84.7%±7.9% versus the positive control 89.8%±4.5% againstYAC-1(P>0.05).The activity of GI-PS could mostly be blocked by ***:GI-PS was shown to be a promising biological response modifier andimmune *** effect of GI-PS on CIK cells is possibly mediated prima-rily through complement receptor type 3.

关键词： Ganoderma lucidum polysaccharides cell proliferation cytotoxicity immunomodula-tion

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Antitumor and anti-angiogenic activity of Ganoderma lucidum polysaccharides peptide

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Acta Pharmacologica Sinica 2004年第6期25卷 131-136页

作者： Qi-zhen CAO, Zhi-bin LIN1 department of Pharmacology, health Science center, {3., beijing 100083, China department of Pharmacology Health Science Center Peking University 100083

AIM: To investigate the antitumor and anti-angiogenic activity of Ganoderma lucidum polysaccharides peptide (GLPP). METHODS: Antitumor effect of GLPP was observed in tumor-bearing mice in vivo. At the same time, the effects of GLPP on proliferation of tumor cells and human umbilical cord vascular endothelial cell (HUVEC) were detected by MTTassay in vitro. Subsequently, spleen lymphocytes proliferation of nude mice was stimulated by LPS or ConA. To investigate the anti-angiogenic effect of GLPP, GLPP 80 μg per disc and GLPP-treated serum 10 μL per disc were added to the chick chorioallantoic membrane (CAM) respectively in vivo. RESULTS: GLPP 50, 100, and 200 mg/kg inhibited growth of Sarcoma 180 in BALB/c mice markedly by 3..2 %, 45.2 %, and 61.9 %, respectively. GLPP which was directly added to the cultured medium did not inhibit PG cell proliferation in vitro; but GLPP-treated serum 50, 100, 200 mg/kg potently inhibited PG cell proliferation by 22.5 %, 26.8 %, and 3..3.%, respectively; and reduced the xenograft (human lung carcinoma cell PG) in BALB/c nude mice greatly in vivo by 55.5 %, 46.0 %, and 46.8 %, respectively. Lymphocytes proliferation of nude mice could be stimulated by LPS 5 mg/Lbut not by ConA 2.5 mg/L, indicating that GLPP could not promote the T lymphocyte proliferation and neutral red phagocytosis of peritoneal macrophages of nude mice. The CAM assay showed that GLPP and GLPP-treated serum had anti-angiogenic effect. GLPP (1, 10, and 100 mg/L) inhibited HUVEC proliferation in vitro with the inhibitory rate of 9.4 %, 15.6 %, and 40.4 %, respectively. CONCLUSION: GLPP has antitumor and anti- angiogenic activity. The anti-angiogenesis of GLPP may be a new mechanism underlying its anti-tumor effects.

关键词： Ganoderma lucidum polysaccharides sarcoma 180 adenocarcinoma lung neoplasms lympho- cyte proliferation peritoneal macrophages angiogenesis nude mice

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Adeno-associated virus-mediated bone morphogenetic protein-7 gene transfer induces C2C12 cell differentiation into osteoblast lineage cells

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Acta Pharmacologica Sinica 2005年第8期26卷 963-968页

作者： Min YANG~2, Qing-jun MA~(2,4), Geng-ting DANG~2, Kang-tao MA~3. Ping CHEN~3. Chun-yan ZHOU~(3.4) ~2department of Orthopedics, peking university Third Hospital, beijing 100083, China ~3.0} of Biochemistry and Molecular Biology, School of Basic medical sciences, peking university health Science center, beijing 100083, China department of Orthopedics Peking University Third Hospital Beijing China department of Biochemistry and Molecular Biology School of Basic Medical Sciences Peking University Health Science Center Beijing China

Aim: To investigate the effects of bone morphogenetic protein-7 (BMP7)-expressing recombinant adeno-associated virus (AAV) vector on the differentiation of C2C12 cells. Methods: AAV-BMP7 was packaged by infecting the stable cell clone BHK-21 (integrated with recombinant AAV vector plasmid pSNAV-BMP7) with recombinant herpes simplex virus type 1, which expresses AAV-2 Rep and Cap and possesses AAV packaging functions. Following infection with AAV-BMP7 at multiplicities of infection of lx 10～5 vector genomes per cell and subse-quent culture, C2C12 cells were assessed qualitatively for BMP7 production, alka-line phosphatase activity, osteocalcin production and Cbfal and MyoD expression. Results: C2C12 cells transduced with AAV-BMP7 could produce BMP7 protein until d 28. Alkaline phosphatase in the cultured C2C12 cell lysate was elevated. Secreted osteocalcin in the culture medium was detectable at d 12 and Cbfal mRNA expression level was upregulated, coinciding with downregulation of MyoD in a temporal manner. Conclusion: The present in vitro study demonstrated that AAV-BMP7 could infect and efficiently convert C2C12 cells from myoblasts into osteoblast lineage cells.

关键词： C2C12 adeno-associated virus bone morphogenetic protein-7 gene therapy

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Real-time detection of α1A-AR movement stimulated by phenylephrine in single living cells

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Acta Pharmacologica Sinica 2007年第6期28卷 796-802页

作者： Ning XU~(2,5),Zhang-yi LIANG~(3.5),Ming XU~2,Ying-hua GUAN~3.Qi-hua HE~4,Qi-de HAN~2,Xin-sheng ZHAO~(3.6),You-yi ZHANG~(2,6)~2 Institute of Vascular Medicine,peking university Third Hospital,and Key Laboratory of Molecular Cardiovascular sciences,Ministry ofEducation,beijing 100083,China ~3.{3. National Laboratory for Molecular sciences,State Key Laboratory for Structural Chemistry ofUnstable and Stable Species,and department of Chemical Biology,College of Chemistry and Molecular Engineering,peking university,{3. 100871,China ~4 center of medical Analysis,peking university,health Science center,beijing 100083,China Institute of Vascular Medicine Peking University Third Hospital and Key Laboratory of Molecular Cardiovascular Sciences Ministry of Education Beijing China beijing National Laboratory for Molecular sciences State Key Laboratory for Structural Chemistry of Unstable and Stable Species department of Chemical Biology College of Chemistry and Molecular Engineering Peking University Beijing China center of medical Analysis Peking University Health Science Center Beijing China

Aim:To investigate the movement of α1A-adrenergic receptors(α1A-AR) stimu-lated by agonist,phenylephrine （PE）,and the dynamics of receptor movement inreal time in single living cells with millisecond ***:We labeledα1A-AR using the monoclonal,anti-FLAG （a kind of tag） antibody and Cy3.conju-gated goat anti-mouse IgG and recorded the trajectory of their transport processin living HEK293. cells stimulated by agonist,PE,and then analyzed their dy-namic ***:The specific detection of α1A-AR on the surface ofliving HEK293.-α1Acells was achieved.α1A-AR internalize under the stimulationof *** the cells were stimulated with PE for 20 min,apparent colocalizationwas found between α1A-AR and *** 40 min stimulation of PE,trajecto-ries of approximate linear motion in HEK293.-α1Acells were recorded,and theirvelocity was ***:The specific labeling method on the livingcell surface provides a convenient means of real-time detection of the behavior ofsurface *** this method we were able to specifically detect α1A-AR andrecord the behavior of individual particles of receptors with 50 ms exposure time inreal time in single living cells.

关键词： adrenergic receptor trajectory living cell

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Role of inositol 1,4,5-trisphosphate receptors in α1-adrenergic receptorinduced cardiomyocyte hypertrophy

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Acta Pharmacologica Sinica 2006年第7期27卷 895-900页

作者： Da-li LUO~(2,3.5) Jian GAO~2 Xiao-mei LAN~3.Gang WANG~4 Sheng WEI~4 Rui-ping XIAO~4 Qi-de HAN~3. department of Pharmacology,School of Chemical Biology & Pharmaceutical sciences,Capital university of {3. sciences,beijing 100069,China 3.Institute of Cardiovascular Science at health Science center,peking university beijing 100083,China 4 Institute of Molecular Medicine and College of Life Science,peking university,beijing 100871,China department of Pharmacology School of Chemical Biology & Pharmaceutical Sciences Capital University of Medical Sciences Beijing China Institute of Cardiovascular Science at health Science center Peking University Beijing China Institute of Molecular Medicine and College of Life Science Peking University Beijing China

Aim:Intracellular Ca2+plays pivotal roles in diverse cellular functions,includinggene transcription that underlies cardiac remodeling during stress ***,the role of inositol 1,4,5-trisphosphate receptors（IP3.s）in the media-tion of cardiac intracellular Ca2+and hypertrophic growth remains *** with neonatal rat ventricular myocytes suggests that activation of IP3.smay be linked to α1adrenergic receptor（α1AR）increased stereotyped Ca2+sparkoccurrence and global Ca2+***,we hypothesized that Ca2+releasethrough IP3.s was necessary for α1AR-stimulated cardiac ***:We used myoinositol 1,4,5-trisphosphate hexakis（butyryloxymethyl）ester（IP3.M）,a membrane-permeant ester of IP3.to activate IP3.s directly,and Fluo 4/AM tomeasure intracellular Ca2+***:IP3.M(10μmol·L-1)mimicked theeffects of phenylephrine,a selective agonist of α1AR,in increments in local Ca2+spark release（especially in the perinuclear area）and global Ca2+*** importantly,IP3. inhibitors,2-aminoethoxydiphenyl borateand Xestospongin C,abolished the IP3.M-induced Ca2+responses,and signifi-cantly suppressed α1AR-induced cardiomyocyte hypertrophy assayed by cellsize,[3.]leucine incorporation and atrial natriuretic factor gene expression,dur-ing sustained（48 h）phenylephrine ***:These results,therefore,provide cellular mechanisms that link IP3. signaling to α1AR-stimulatedgene expression and cardiomyocyte hypertrophy.

关键词： inositol 1,4,5-trisphosphate receptors Ca2+sparks α1 adrenergic stimulation cardiac hypertrophy

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Status of study on biological and toxicological effects of nanoscale materials

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Science China Chemistry 2005年第5期48卷 385-394页

作者： WANG Bing1, FENG Weiyue1, ZHAO Yuliang1, XING Gengmei1, CHAI Zhifang1, WANG Haifang2 & JIA Guang3.1. Laboratory for Bio-Environmental health sciences of Nanoscale Materials (Nanosafety Lab), Institute of High Energy Physics, Chi-nese Academy of sciences, {3. 100049, China 2. College of Chemistry and Molecular Engineering, peking university, {3. 100871, China 3. department of Occupational and Environmental health sciences, School of Public health, peking university, beijing 100083, China Laboratory for Bio-Environmental health sciences of Nanoscale Materials (Nanosafety Lab) Institute of High Energy Physics Chinese Academy of Sciences Beijing China College of Chemistry and Molecular Engineering Peking University Beijing China department of Occupational and Environmental health sciences School of Public Health Peking University Beijing China

Because the physical and chemical properties of nanosized materials mostly differ from the existing microsized materials, their potential impacts on human health and the envi-ronment will be topics under the serious discussions in press and in a number of international scientific journals. We analyze and summarize the existing data of the experimental study on the biological activities and adverse effects of nanoscale materials/particles including single wall carbon nanotubes, multi wall carbon nanotubes, titanium oxide and iron powders. Though some biological behaviors of nanoscale materials observed cannot be understood on the basis of the current knowledge, as the existing data are mostly preliminary, it is too early to make some ex-clusive conclusions on biological activities (or the toxicity) of any of nanoscale materials. The experimental techniques, the current topics, and the future research directions for this new re-search field are also discussed.

关键词： nanomaterials, single wall carbon nanotubes, multi wall carbon nanotubes, titanium oxide and iron, biological activity and toxicological effect.

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