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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~32.Department of Pharmacology,School of Chemical Biology & pharmaceutical sciences,Capital{2. of Medical sciences,Beijing 100069,China 3 Institute of Cardiovascular Science at Health Science Center,Peking{2. Beijing 100083,China 4 Institute of Molecular Medicine and college of Life Science,Peking{2.,Beijing 100871,China Department of Pharmacology School of Chemical Biology & Pharmaceutical Sciences Capital University of Medical Sciences Beijing 100069 China Institute of Cardiovascular Science at Health Science Center Peking University Beijing 100083 China Institute of Molecular Medicine and college of Life Science Peking University Beijing 100871 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（IP3Rs）in the media-tion of cardiac intracellular Ca2.and hypertrophic growth remains *** with neonatal rat ventricular myocytes suggests that activation of IP3Rsmay be linked to α1adrenergic receptor（α1AR）increased stereotyped Ca2.sparkoccurrence and global Ca2.***,we hypothesized that Ca2.releasethrough IP3Rs was necessary for α1AR-stimulated cardiac ***:We used myoinositol 1,4,5-trisphosphate hexakis（butyryloxymethyl）ester（IP3BM）,a membrane-permeant ester of IP3,to activate IP3Rs directly,and Fluo 4/AM tomeasure intracellular Ca2.***:IP3BM(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,IP3R inhibitors,2.aminoethoxydiphenyl borateand Xestospongin C,abolished the IP3BM-induced Ca2.responses,and signifi-cantly suppressed α1AR-induced cardiomyocyte hypertrophy assayed by cellsize,[3H]leucine incorporation and atrial natriuretic factor gene expression,dur-ing sustained（48 h）phenylephrine ***:These results,therefore,provide cellular mechanisms that link IP3R signaling to α1AR-stimulatedgene expression and cardiomyocyte hypertrophy.

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

Propranolol and verapamil inhibit mRNA expression of RyR2.and SERCA in L-thyroxin-induced rat ventricular hypertrophy

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Acta Pharmacologica Sinica 2004年第03期25卷 93-97页

作者： rat ventricular hypertrophy1 Xiao-dong WU2.De-zai DAI2.Qiu-pin ZHANG3,Feng GAO3 Research Division of Pharmacology,China pharmaceutical university 3Laboratorial Center ofMedicine,Southeast university,Nanjing 2.0009,China Research Division of Pharmacology China Pharmaceutical University Laboratorial Center of Medicine Southeast University

AIM: To study the alteration in the mRNA level of cardiac ryanodine receptor 2.(RyR2. and sarco-endoplasmic reticulum Ca2.-ATPase (SERCA) in L-thyroxin-induced hypertrophy. METHODS: L-thyroxin (500 g/kg) daily was injected for 10 d. RT-PCR was used to determine mRNA expression. RESULTS: An increase in the relative amount of RyR2.(111 %) and SERCA mRNA (65 %) expression was observed in the hypertrophied rats (RyR2. 77±11; SERCA: 87±10, n=9) compared with the normal rats (RyR2. 36±10; SERCA: 53±10, n=9). Propranolol was effective to inhibit the increase in RyR2.(51±7) and SERCA (63±13) mRNA expression in hypertrophied rats, respectively. Verapamil also reduced RyR2.(62.5) and SERCA (75±8) mRNA expression. CONCLUSION: Both RyR2.and SERCA mRNA level in L-thyroxin-induced cardiac hypertrophy was over-expressed and propranolol or verapamil inhibited the alteration.

关键词： heart hypertrophy arrhythmia ryanodine receptors Ca2.-transporting ATPase L-thyroxin propranolol verapamil reversed transcriptase polymerase chain reaction

Prediction, Synthesis and Antigenicity of the Antigenic Peptides of 2.kDa Glutathione S-Transferasc of Schistosoma Japonicum (Sj2.)

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Chinese Chemical Letters 1999年第1期10卷 27-28页

作者： Jia Xi XU Meng Shen CAI(college of Chemistry and Molecular Engineering, Peking university, Beijing 100871)(School of{2. sciences, Beijing Medical university. Beijing 100083) Coll. of Chem. and Molec. Eng. Peking University Beijing 100871 China School of pharmaceutical sciences Beijing Medical University Beijing 100083 China

Six antigenic peptides of 2. kDa glutathione S-transferase of Schistosoma japonicum(Sj2.) have been predicted according to their hydrophilicity, flexibility. accessibility. chargedistribution and β -turn in the secondary structure by the determination of its primary structure andsynthesized by solid phase method. All of them showed antigenicity with anti-schistosomajaponicum immunoglobulin polyclonal antibody, anti-Sj-lgG PcAb by Dot-ELISA. Three of themshowed good antigenicity. They would serve as candidates of synthetic anti-schistosomal vaccine.

关键词： SchistosomajQPonicum glutathione S-transferase antigenic peptide peptide vaccine.

Synthesis and Antifungal Activity of Novel 1,2.4-Triazole Derivatives

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Synthesis and Antifungal Activity of Novel 1,2,4-Triazole De...

Rapid quantification of the metabolite of valacyclovir hydrochloride in human plasma by liquid chromatography-tandem mass spectrometry

第六届全国化学生物学学术会议

作者： Kun Wan~Ⅰ,Jia-li Mi~Ⅱ,Cheng-he Zhou~(Ⅰ,Ⅱ*)ⅠSchool of Chemistry and Chemical Engineering,southwest university,{2. 400715Ⅱcollege of pharmaceutical sciences,{2. Medical university,{2. 400016

＜正＞Triazole antifungal agents such as fluconazole now play a leading role in the treatment of invasive fungal ***,the increasing administration of such antifungal agents has led to the development of fungal *** rev... 详细信息

关键词： Triazole Synthesis Antifungal

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Journal of pharmaceutical Analysis 2010年第2期22卷 83-90页

作者： Yuan Tian1,2.Hui Lin1,2.Xue-Yu Zhang1,2.Zun-Jian Zhang1,2.Guo-Guang Mao31. Key Laboratory of Drug Quality Control and Pharmacovigilance (China pharmaceutical university),Ministry of Education,Nanjing 2.0009 2. Center for Instrumental Analysis,China pharmaceutical university,Nanjing 2.0009 3. Department of Clinical Pharmacology,Wannan Medical college,Wuhu 2.1000,China. Key Laboratory of Drug Quality Control and Pharmacovigilance (China pharmaceutical university) Ministry of Education Nanjing 210009 China Center for Instrumental Analysis China Pharmaceutical University Nanjing 210009 China Department of Clinical Pharmacology Wannan Medical College Wuhu 241000 China

Objective To establish a rapid,sensitive and selective liquid chromatography-tandem mass spectrometry (LC-MS/MS) method for the determination of acyclovir (the metabolite of valacyclovir hydrochloride) in human plasma. Methods After addition of ganciclovir as internal standard (IS),plasma samples were prepared by one-step protein precipitation using acetonitrile as precipitant,followed by an isocratic elution with 0.1% formic acid solution-methanol (95∶5,v/v) on an Agilent ZORBAX SB-C18 (150mm×2.1mm i.d.,3.5μm) column. Detection was performed on a triple-quadrupole mass spectrometer utilizing electrospray ionization (ESI) interface operating in positive ion and selected reaction monitoring (SRM) mode with the precursor to product ion transitions m/z 2.6.2.152.1 for acyclovir and m/z 2.6.2.152.1 for the IS. Results The analytical results demonstrated a good linearity over the ranges from 0.005 to 4μg/mL (r=0.9999) for valacyclovir hydrochloride. The relative standard deviations (RSD) of intra-batch and inter-batch were less than 4.06% and 9.2.%,respectively. The limit of detection and lower limit of quantification in human plasma were 2.g/mL and 5ng/mL,respectively. Conclusion The method was simple,sensitive,accurate and reproducible and has been successfully applied to a bioequivalence study of valacyclovir hydrochloride capsules in Chinese healthy male volunteers.

关键词： valacyclovir hydrochloride acyclovir liquid chromatography-tandem mass spectrometry method validation human plasma

Dispersion of ventricular mRNA of RyR2.and SERCA2.associated with arrhythmogenesis in rats

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Acta Pharmacologica Sinica 2004年第6期25卷 36-41页

作者： Hong-lan WANG, De-zai DAI2. Feng GAO3, Yan-pin ZHANG3, Feng LU Research Division of Pharmacology, China pharmaceutical university, Nanjing 2.0009, China 3Laboratorial Center ofMedicine, Southeast university, Nanjing 2.0009, China Research Division of Pharmacology China Pharmaceutical University Nanjing 210009 China

AIM: To investigate the effect of CPU86017 on the changes of mRNA abundance of different calcium handling system in infarcted heart. METHODS: Rats were subjected to left coronary ligation to induce myocardial infarc- tion (MI). The treatment with either propranolol (Pro) 5 mg/kg ip or CPU86017 1, 2. and 4 mg/kg ip was initiated on the next day of operation and continued for 2. d. Medication with isoproterenol (Isop) 3 mg/kg sc started on the d 17-2.. Ventricular mRNA abundance of ryanodine receptor 2.(RyR2., sarcoplasmic reticulum Ca2.-ATPase (SERCA2., L-type Ca2. channel, and Na+/Ca2.exchanger (NCX1) were measured. RESULTS: Arrhythmic scores (AS) in the Isop group was raised up to 5.2.±1.75 (P2.2.±2.04 and sham group 1.50±1.73. The AS was depressed by Pro (1.63±1.53, P2.and 4 mg/kg (3.00±1.2., and 1.70±1.85, P2. and SERCA2.was associated with an increase in AS in Isop group, and it was much depressed in the left than the right ventricle. The dispersion and depression of mRNA were restored significantly by Pro and CPU86017, asso- ciated with suppression on AS. In Isop group, the mRNA abundance of L-type Ca2. channel was not changed; and a moderate increase in the mRNA of NCX1 was seen, the changes were regressed by Pro and CPU86017. CONCLUSION: Isop-induced arrhythmogenesis in MI heart was correlated mainly with a dispersion of depressed mRNA abundance in ventricle likely due to the consequence of PKA over-phosphorylation. A suppression of arrhythmia by Pro and CPU86017 resulted from a regression of the dispersion and depression of RyR2.and SERCA2.

关键词： myocardial infarction isoproterenol arrhythmia calcium 4-chlorobenzyltetrahydroberberine

Binding activity of H-Ras is necessary for in vivo inhibition of ASK1 activity

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Cell Research 2004年第2期14卷 148-154页

作者： Jun DU~(1,2.), Shao Hui CAI~(3,4), Zhe SHI~3, Fumihiko NAGASE~1 ~1Department of Medical Technology, Nagoya university School of Health sciences, Aichi 461-8673, Japan. ~2.chool of{2. Science, Sun Yat-Sen university, Guangzhou, 510089, China. ~3Department of Immunology, Nagoya university Graduate and Faculty School of Medicine, Aichi, 466-8550, Japan. ~4college of Pharmacy, Jinan university, Guangzhou, 510632. China. 2.chool of pharmaceutical Science Sun Yat-Sen University Guangzhou 510089 China. 4college of Pharmacy Jinan University Guangzhou 510632 China. 3Department of Immunology Nagoya University Graduate and Faculty School of Medicine Aichi 466-8550 Japan. 1Department of Medical Technology Nagoya University School of Health Sciences Aichi 461-8673 Japan.

H-Ras is well known as one of the essential components of Ras/Raf/MEK/ERK cascade, which is a critical prosurvival signaling mechanism in most eukaryotic cells. Ras targets Raf/MEK/ERK cascade by integrating and transmitting extracellular signals from growth factor receptors to Raf, leading to the propagation of signals to modulate a serious of cellular survival events. Apoptosis signal-regulating kinasel (ASK1) serves as a general mediator of cell death because it is responsive to a variety of death signals. In this study, we found that H-Ras interacted with ASK1 to cause the inhibition of both ASK1 activity and ASK1-induced apoptosis in vivo, which was reversed only partially by addition of RafS62.A, an antagonist of Raf, whereas MEK inhibitor, PD98059, and PI3K inhibitor, LY2.4002. did not disturb the inhibitory effect of H-Ras on ASK-1-induced apoptosis. Furthermore, by means of immunoprecipitate and kinase assays, we demonstrated that the interaction between H-Ras and ASK1 as well as the inhibition

关键词： H-Ras ASK1 apoptosis binding activity.

Investigation of the differences between the “COLD” and “HOT” nature of Coptis chinensis Franch and its processed materials based on animal’s temperature tropism

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Science China(Life sciences) 2009年第11期52卷 1073-1080页

作者： ZHOU CanPing1,2. WANG JiaBo1, ZHANG XueRu1,2. ZHAO YanLing1, XIA XinHua2. ZHAO HaiPing1, REN YongShen1 & XIAO XiaoHe1 1 China Military Institute of Chinese Meteria Medica, 302.Military Hospital of China, Beijing 100039, China 2.college of pharmaceutical{2., Hunan university of Chinese Medicine, Changsha 4102.8, China China Military Institute of Chinese Meteria Medica 302 Military Hospital of China Beijing 100039 China college of pharmaceutical{2. Hunan University of Chinese Medicine Changsha 410208 China

The description and differentiation of the so-called "Cold" and "Hot" natures, the primary "Drug Naure" of Chinese medicine, is the focus of theoretical research. In this study, the divergency between the "Cold" and the "Hot" natures was investigated through examining the temperature tropism of mice affected by Coptis chinensis Franch and its processed materials by using a cold/hot plate differentiating technology. After exposure to C. chinensis Franch, the macroscopic behavioral index of the remaining rate (RR) on a warm pad (40℃ ) significantly increased (P<0.05), suggesting the enhancement of Hot tropism. The internal indexes of adenosine triphosphatase (ATPase) activity and oxygen consuming volume decreased significantly (P<0.05), suggesting the decapability of energy metabolism. This external behavior of Hot tropism might reflect the internal Cold nature of C. chinensis Franch. However, the processed materials of C. chinensis Franch exhibited a different Cold nature in temperature tropism compared with crude C. chinensis Franch (CC): the Cold nature of bile-processed C. chinensis Franch (BC) enhanced while the ginger-processed C. chinensis Franch (GC) changed inversely. The changing sequence was consistent with the theoretical prognostication. It is indicated that the external Cold & Hot natures of Chinese medicine may possibly reflect in an ethological way for the changes of animal’s temperature tropism which might be internally regulated by the body’s energy metabolism.

关键词： "Cold" and "Hot" natures of Chinese medicine evaluation temperature tropism ethology drug process Coptis chinensis Franch

Endothelin-1 induces intracellular [Ca^(2.)] increase via Ca^(2.) influx through the L-type Ca^(2.) channel, Ca^(2.)-induced Ca^(2.) release and a pathway involving ET_A receptors, PKC, PKA and AT1 receptors in cardiomyocytes

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Science China(Life sciences) 2009年第4期52卷 360-370页

作者： ZENG QingHua1, LI XingTing1, ZHONG GuoGan2. ZHANG WenJie2.& SUN ChengWen3 1 Laboratory of Molecular & Cellular Physiology, School of Life sciences, Northeast Normal university, Changchun 13002., China 2.Department of Physiology, School of Basic Medical sciences, Jilin university, Changchun 13002., China 3 Department of pharmaceutical sciences, North Dakota State university, Fargo, NorthDakota, USA Laboratory of Molecular & Cellular Physiology School of Life Sciences Northeast Normal University Changchun 130024 China Department of Physiology School of Basic Medical Sciences Jilin University Changchun 130021 China Department of pharmaceutical sciences North Dakota State University Fargo NorthDakota USA

Using fura-2.acetoxymethyl ester (AM) fluorescence imaging and patch clamp techniques, we found that endothelin-1 (ET-1) significantly elevated the intracellular calcium level ([Ca2.]i) in a dose-dependent manner and activated the L-type Ca2. channel in cardiomyocytes isolated from rats. The effect of ET-1 on [Ca2.]i elevation was abolished in the presence of the ETA receptor blocker BQ12., but was not affected by the ETB receptor blocker BQ788. ET-1-induced an increase in [Ca2.]i, which was inhibited 46.7% by pretreatment with a high concentration of ryanodine (10 μmol/L), a blocker of the ryanodine receptor. The ET-1-induced [Ca2.]i increase was also inhibited by the inhibitors of protein kinase A (PKA), protein kinase C (PKC) and angiotensin type 1 receptor (AT1 receptor). We found that ET-1 induced an enhancement of the amplitude of the whole cell L-type Ca2. channel current and an increase of open-state probability (NPo) of an L-type single Ca2. channel. BQ12. completely blocked the ET-1-induced increase in calcium channel open-state probability. In this study we demonstrated that ET-1 regulates calcium overload through a series of mechanisms that include L-type Ca2. channel activation and Ca2.-induced Ca2. release (CICR). ETA receptors, PKC, PKA and AT1 receptors may also contribute to this pathway.

关键词： endothelin-1(ET-1) cardiomyocytes intracellular calcium concentration ([Ca2.]i) L-type Ca2. channel current (ICaL) Ca2.-induced Ca2. release (CICR) ETA receptors PKC PKA AT1 receptors