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

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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Expression of PDCD5 , a novel apoptosis related protein, in human osteoarthritic cartilage

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Acta Pharmacologica Sinica 2004年第5期25卷 143-148页

作者： Ai-xin CHENG, Si-quan LOU2, Hao-wei ZHOU, Ying WANG3, Da-long MA3department of Orthopaedic Surgery, third hospital, peking university, beijing 100083 3Center for Human Disease Genomics, peking university, beijing 100083, china department of Orthopaedic Surgery Third Hospital Peking University 北京 100083 Center for Human Disease Genomics Peking University 北京 100083

AIM: To investigate the expression features of PDCD5 (programmed cell death 5 protein) in osteoarthritic andnormal human cartilage, and speculate on its potential functions in the pathogenesis of osteoarthritis (OA).METHODS: Articular cartilage specimens were obtained from 30 patients with OA and 16 healthy patients at thetime of arthroplasty. Expression of PDCD5 was detected by flow cytometry, immunofluorescence, RT-PCR andimmunohistochemical analysis. RESULTS: Enhanced expression and nuclear accumulation of PDCD5 in OAchondrocytes were found. PDCD5-positive chondrocytes were mainly distributed in the superficial and deep zonesof OA tissue sections, as opposed to, in the superficial and middle regions of normal healthy tissue ***: Since apoptotic chondrocyte death occurs more frequently in OA cartilage than in normal healthycartilage and PDCD5 is an apoptosis-related protein, the different expression patterns of PDCD5 in OA cartilagefrom that in normal healthy cartilage indicate that PDCD5 is involved in the pathogenesis of OA.

关键词： apoptosis cartilage osteoarthritis PDCD5

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Up-regulation of Cartilage Oligomeric Matrix Protein Gene Expression by Insulin-like Growth Factor-Ⅰ Revealed by Real Time Reverse Transcription-Polymerase Chain Reaction

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Acta Biochimica et Biophysica Sinica 2006年第10期38卷 677-682页

作者： Hua TIAN~(1,2*) Ioannis STOGIANNIDIS~2 1 department of Orthopaedics,peking university third hospital,beijing 100083,china 2 Coxa hospital for Joint Replacement,Biokatu 6 b,Tampere 33101,Finland department of Orthopaedics Peking University Third HospitalBeijing 100083 China Coxa hospital for Joint Replacement Biokatu 6 bTampere 33101 Finland

Cartilage oligomeric matrix protein (COMP) strengthens cartilage by binding to type Ⅱ and typeⅨ collagen-forming bridges between collagen *** was hypothesized that perhaps one or more anabolicgrowth factors such as insulin-like growth factor-Ⅰ (IGF-Ⅰ),fibroblast growth factor-1 (FGF-1) or plateletderived growth factor-BB (PDGF-BB) increase COMP gene *** effects on primary humanchondrocytes and the chondrogenic cell line ATDC5 were studied using real time reverse transcript-poly-merase chain reaction (RT-PCR) for ***-Ⅰ,but not the FGF-1 or PDGF-BB,up-regulatedCOMP gene expression by approximate 5-fold in human adult chondrocytes in a dose-and ***-Ⅰ exerted similar effects on ATDC5 *** from these real time RT-PCR experimentswere confirmed by transfecting into ATDC5 cells a full-length mouse COMP promoter cloned upstream of aluciferase reporter *** stimulation with IGF-Ⅰ,the luciferase reporter activity increased by about *** conclusion,IGF-Ⅰ seems to be an important positive regulator of COMP,which may play animportant role in an attempted repair of either traumatized or degenerated cartilage.

关键词： cartilage oligomeric matrix protein (COMP) insulin-like growth factor-Ⅰ(IGF-Ⅰ) gene expression

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THE PHYSICAL ENTROPY OF SINGLE CONSERVATION LAWS

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Journal of Computational Mathematics 1998年第5期16卷 437-444页

作者： (department of Mathematics, peking university, beijing 100871, china) 北京大学数学系北京

By means of the comparisons with the formulas in statistical mechanics and thermodynamics, in this paper it is demonstrated that for the single conservation law partial derivative(t)u + partial derivative(x)f(u) = 0, if the flux function f(u) is convex (or concave), then, the physical entropy is S = -f(u); Furthermore, if we assume this result can be generalized to any f(u) with two order continuous derivative, from the thermodynamical principle that the local entropy production must be non-negative, one entropy inequality is derived, by which the O.A. Olejnik's famous E- condition can be explained successfully in physics.

关键词： conservation laws entropy entropy production

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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 ~3department 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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Beneficial metabolic effects of nateglinide versus acarbose in patients with newly-diagnosed type 2 diabetes

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Acta Pharmacologica Sinica 2007年第4期28卷 534-539页

作者： Hong-wei GAO Chao XIE Hai-ning WANG Yu-jing LIN Tian-pei HONG department of Endocrinology,peking university third hospital,beijing 100083,china department of Endocrinology Peking University Third Hospital Beijing China

Aim:To investigate the acute and chronic effects of nateglinide versus acarboseon plasma asymmetric dimethylarginine (ADMA) levels and lipid profiles inpatients with newly-diagnosed type 2 ***:A crossover trial ofnateglinide and acarbose was conducted on 16 drug-nave patients with newly-diagnosed type 2 diabetes during a total period of 9 *** glucose,seruminsulin,free fatty acids (FFA),lipids and lipoproteins,and plasma ADMA ***:The efficiencies of a single dose of nateglinide (120 mg) andacarbose (50 mg) for lowering postprandial hyperglycemia were ***-pared to acarbose,nateglinide significantly increased postprandial insulin releaseafter a standard meal test in patients with type 2 *** acutelydecreased postprandial 120 min FFA concentrations and 240 min ADMA levelsmore significantly than *** fasting high-density lipoprotein choles-terol level increased and the low-density lipoprotein cholesterol level decreasedsignificantly,but the fasting levels of triglycerides,total cholesterol,and ADMAwere unchanged after 4 weeks of treatment with *** did notaffect fasting lipid profiles or the ADMA levels after 4 weeks of ***:These results suggest that the reduction of postprandial FFA andADMA concentrations induced by nateglinide may be associated with the partialrestoration of early-phase insulin secretion and may impart a cardiovascularadvantage in comparison with acarbose.

关键词： nateglinide acarbose free fatty acids asymmetric dimethylarginine

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Overexpression of heme oxygenasel protects smooth muscle cells against oxidative injury and inhibits cell proliferation

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Cell Research 2002年第2期12卷 123-132页

作者： MIN ZHANG, BAO HuI ZHANG, LI CHEN, WEI AN1 Institute of Sports Medicine, The third hospital, peking university, beijing 100083, china 2department of Cell Biology, Capital university of Medical Sciences, beijing 100054, china Institute of Sports Medicine The Third Hospital Peking University Beijing China department of Cell Biology Capital University of Medical Sciences Beijing China

To investigate whether the expression of exogenous heme oxygenase-1 (HO-1) gene within vascular smooth muscle cells (VSMC) could protect the cells from free radical attack and inhibit cell proliferation, we established an in vitro transfection of human HO-1 gene into rat VSMC mediated by a retroviral vector. The results showed that the profound expression of HO-1 protein as well as HO activity was 1.8- and 2.0-fold increased respectively in the transfected cells compared to the non-transfected ones. The treatment of VSMC with different concentrations of H2O2 led to the remarkable cell damage as indicated by survival rate and LDH leakage. However, the resistance of the HO-1 transfected VSMC against H2O2 was significantly raised. This protective effect was dramatically diminished when the transfected VSMC were pretreated with ZnPP-IX, a specific inhibitor of HO, for 24 h. In addition, we found that the growth potential of the transfected cells was significantly inhibited directly by increased activity of H

关键词： Heme oxygenase retroviral vector free radical cell proliferation vascular smooth muscle cells.

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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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Population pharmacokinetics of valproate in Chinese children with epilepsy

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Acta Pharmacologica Sinica 2007年第10期28卷 1677-1684页

作者： De-chun JIANG~(2,3),Li WANG~4,Yu-qin WANG~(2,6),Lin LI~3,Wei LU~5,Xiang-rong BAI~2~2 department of Pharmacy,Xuan-wu hospital of Capital Medical university,beijing 100053,china ~4 department of Pediatrics,peking universityFirst hospital,beijing 100034,china ~3 department of Pharmacology,Xuan-wu hospital of Capital Medical university,Education Ministry KeyLaboratory for Neurodegenerative Diseases,beijing 100053,china ~5 School of Pharmaceutical Science,peking university,beijing 100083,china department of Pharmacy Xuan-wu Hospital of Capital Medical University Beijing China department of Pharmacology Xuan-wu Hospital of Capital Medical University Education Ministry Key Laboratory for Neurodegenerative Diseases Beijing China department of Pediatrics Peking University First Hospital Beijing China School of Pharmaceutical Science Peking University Beijing China

Aim:The aim of the present study is to establish a population pharmacokinetic（PPK） model of valproate （VPA） in Chinese epileptic children to promote thereasonable use of anti-epileptic ***:Sparse data of VPA serumconcentrations from 417 epileptic children were *** patients weredivided into 2 groups:the PPK model group （n=317） and the PPK valid group（n=100）.The PPK parameter values of VPA were calculated by NONMEM soft-ware using the data of the PPK model group.A basic model and a final modelwere set *** validate the 2 models,the concentrations of PPK valid groupwere predicted by each model,*** mean prediction error （MPE）,mean squared prediction error （MSPE）,root mean squared prediction error（RMSPE）,weight residues （WRES）,and the 95% confidence intervals （95%CI） were also ***,the values between the 2 models were ***:The PPK of VPA was determined by a 1-compartment model with afirst-order absorption *** basic model was:Ka=3.09 (h-1),V/F=20.4（L）,CL/F=0.296 （L/h）.The final model was:Ka=0.251+2.24·（1-HS）(h-1),V/F=2.88+0.157·WT （L）,CL/F=0.1060.98·CO+0.0157·AGE （L/h）.For thebasic model,the MPE,MSPE,RMSPE,WRES,and the 95% CI were-23.53（-30.36,-16.70）,3728.96 （2872.72,4585.20）,39.62 （34.34,44.90）,and-0.06 （-0.14,0.02）,*** the final model,the MPE,MSPE,RMSPE,WRES,and the95% CI were-1.16 （-4.85,2.53）,1002.83 （1050.64,1143.61）,23.04 （21.12,24.96）,and0.08 （-0.04,0.20）,*** final model was more optimal than the ***:The PPK model of VPA in Chinese epileptic children wassuccessfully *** will be valuable to facilitate individualized dosageregimens.

关键词： population pharmacokinetics valproic acid epilepsy children Bayesian method NONMEM software individualized dosage regimens

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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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