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胶束动电毛细管色谱法测定三磷酸腺苷制剂含量 被引量:4
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作者 郭郁 马捷 +1 位作者 刘志鹤 南国柱 《药物分析杂志》 CAS CSCD 北大核心 1998年第2期106-109,共4页
应用胶束动电毛细管色谱法测定三磷酸腺苷(ATP)制剂的含量,同时还可测出所含二磷酸腺苷(ADP)及一磷酸腺苷(AMP).测定运行液采用pH=9.5的0.02mol/L磷酸盐缓冲液,其中含0.1mol/L胆酸钠,恒定电... 应用胶束动电毛细管色谱法测定三磷酸腺苷(ATP)制剂的含量,同时还可测出所含二磷酸腺苷(ADP)及一磷酸腺苷(AMP).测定运行液采用pH=9.5的0.02mol/L磷酸盐缓冲液,其中含0.1mol/L胆酸钠,恒定电压16kV(运行电流145~155μA).各组分的迁移时间(tM)在10~20min之内.选择对氨基苯磺酸钠作内标,各组分浓度在0.1~2.0g/L范围内对内标峰面积之比呈良好线性关系.样品各组分的批内RSD<3%(n=9),回收率为99.10%~101.4%,RSD<3%(n=5).与药品标准的测定方法相比较,ATP测定值最大相差为3.3%,但前者不能测定其它成分. 展开更多
关键词 胶束动电 毛细管色谱 atp制剂 含量测定
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Sulfide-based ATP production in Urechis unicinctus
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作者 马卓君 包振民 +1 位作者 王思锋 张志峰 《Chinese Journal of Oceanology and Limnology》 SCIE CAS CSCD 2010年第3期521-526,共6页
We measured sulfide-based ATP production by isolated mitochondria from four tissues of Urechis unicinctus and the effects of inhibitors of respiratory complexes on ATP production were evaluated. The results show that ... We measured sulfide-based ATP production by isolated mitochondria from four tissues of Urechis unicinctus and the effects of inhibitors of respiratory complexes on ATP production were evaluated. The results show that these mitochondria could oxidize sulfide to produce ATP. The yield of sulfide-stimulated ATP varied from 5 nmol ATP/min/mg to 90 nmol ATP/min/mg according to the sulfide concentration and the source of the mitochondria. The maximum ATP synthesis occurred in hindgut mitochondria using 5 μmol/L sulfide as a substrate. The effects of inhibitors (Rotenone, Antimycin A, Cyanide, and Salicylhydroxamic acid) on mitochondrial ATP production varied with the source of the mitochondria. Our results indicate that sulfide-based ATP production and the associated electron transport pathway are tissue-specific in U. unicinctus. 展开更多
关键词 Urechis unicinctus sulfide oxidation MITOCHONDRIA atp production INHIBITOR
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S100A8/A9 induces autophagy and apoptosis via ROS-mediated cross-talk between mitochondria and lysosomes that involves BNIP3 被引量:14
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作者 Saeid Ghavami Mehdi Eshragi +7 位作者 Sudharsana R Ande Walter J Chazin Thomas Klonisch Andrew J Halayko Karol D Mcneill Mohammad Hashemi Claus Kerkhoff Marek Los 《Cell Research》 SCIE CAS CSCD 2010年第3期314-331,共18页
The complex formed by two members of the S100 calcium-binding protein family, S100A8/A9, exerts apoptosisinducing activity in various cells of different origins. Here, we present evidence that the underlying molecular... The complex formed by two members of the S100 calcium-binding protein family, S100A8/A9, exerts apoptosisinducing activity in various cells of different origins. Here, we present evidence that the underlying molecular mechanisms involve both programmed cell death I (PCD I, apoptosis) and PCD II (autophagy)-like death. Treatment of cells with S100A8/A9 caused the increase of Beclin-1 expression as well as Atgl2-Atg5 formation. S100A8/A9-induced cell death was partially inhibited by the specific PI3-kinase class Ⅲ inhibitor, 3-methyladenine (3-MA), and by the vacuole H+-ATPase inhibitor, bafilomycin-A1 (Baf-A1). S100A8/A9 provoked the translocation of BNIP3, a BH3 only pro-apoptotic Bcl2 family member, to mitochondria. Consistent with this finding, ATM-BNIP3 overexpression partially inhibited S100A8/A9-induced cell death, decreased reactive oxygen species (ROS) generation, and partially pro- tected against the decrease in mitochondrial transmembrane potential in S100A8/A9-treated ceils. In addition, either ATM-BNIP3 overexpression or N-acetyl-L-cysteine co-treatment decreased lysosomal activation in cells treated with S100A8/A9. Our data indicate that S100A8/A9-promoted cell death occurs through the cross-talk of mitochondria and lysosomes via ROS and the process involves BNIP3. 展开更多
关键词 S100A8/A9 CALPROTECTIN lysosomal activation mitochondrial membrane potential BNIP3 BECLIN-1
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Effects of prostaglandin F_(2α) on small intestinal interstitial cells of Cajal 被引量:1
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作者 Chan Guk Park Young Dae Kim +5 位作者 Man Yoo Kim Jae Woong Koh Jae Yeoul Jun Cheol Ho Yeum Insuk So Seok Choi 《World Journal of Gastroenterology》 SCIE CAS CSCD 2011年第9期1143-1151,共9页
AIM:To explore the role of prostaglandin F2α(PGF2α) on pacemaker activity in interstitial cells of Cajal(ICC)from mouse small intestine. METHODS:In this study,effects of PGF2αin the cultured ICC cells were in... AIM:To explore the role of prostaglandin F2α(PGF2α) on pacemaker activity in interstitial cells of Cajal(ICC)from mouse small intestine. METHODS:In this study,effects of PGF2αin the cultured ICC cells were investigated with patch clamp technology combined with Ca 2+ image analysis. RESULTS:Externally applied PGF2α(10μmol/L)produced membrane depolarization in current-clamp mode and increased tonic inward pacemaker currents in voltage-clamp mode.The application of flufenamic acid(a non-selective cation channel inhibitor)or niflumic acid(aCl channel inhibitor)abolished the generation of pacemaker currents but only flufenamic acid inhibited the PGF2α-induced tonic inward currents.In addition,the tonic inward currents induced by PGF2αwere not inhibited by intracellular application of 5’-[-thio]diphosphate trilithium salt.Pretreatment with Ca 2+ free solution, U-73122,an active phospholipase C inhibitor,and thapsigargin,a Ca 2+ -ATPase inhibitor in endoplasmic reticulum,abolished the generation of pacemaker currents and suppressed the PGF2α-induced tonic inward currents.However,chelerythrine or calphostin C,protein kinase C inhibitors,did not block the PGF2α-induced effects on pacemaker currents.When recording intracellular Ca 2+ ([Ca 2+ ]i)concentration using fluo-3/AM,PGF2α broadly increased the spontaneous[Ca 2+ ]i oscillations. CONCLUSION:These results suggest that PGF2αcan modulate pacemaker activity of ICC by acting non-selective action channels through phospholipase C-dependent pathway via[Ca2+]i regulation 展开更多
关键词 Prostaglandin F2α Interstitial cells of Cajal Tonic inward currents Intestinal motility
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Mechanisms of cholecystokinin-induced calcium mobilization in gastric antral interstitial cells of Cajal 被引量:2
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作者 Yao-Yao Gong Xin-Min Si +1 位作者 Lin Lin Jia Lu 《World Journal of Gastroenterology》 SCIE CAS CSCD 2012年第48期7184-7193,共10页
AIM:To investigate the effect of sulfated cholecystokinin-8(CCK-8S) on calcium mobilization in cultured murine gastric antral interstitial cells of Cajal(ICC) and its possible mechanisms.METHODS:ICC were isolated from... AIM:To investigate the effect of sulfated cholecystokinin-8(CCK-8S) on calcium mobilization in cultured murine gastric antral interstitial cells of Cajal(ICC) and its possible mechanisms.METHODS:ICC were isolated from the gastric antrum of mice and cultured.Immunofluorescence staining with a monoclonal antibody for c-Kit was used to identify ICC.The responsiveness of ICC to CCK-8S was measured using Fluo-3/AM based digital microfluorimetric measurement of intracellular Ca2+ concentration([Ca2+]i).A confocal laser scanning microscope was used to monitor [Ca2+]i changes.The selective CCK1 receptor antagonist lorglumide,the intracellular Ca2+-ATPase inhibitor thapsigargin,the type Ⅲ inositol 1,4,5-triphosphate(InsP3) receptor blocker xestospongin C and the L-type voltage-operated Ca2+ channel inhibitor nifedipine were used to examine the mecha-nisms of [Ca2+]i elevation caused by CCK-8S.Immunoprecipitation and Western blotting were used to determine the regulatory effect of PKC on phosphorylation of type Ⅲ InsP3 receptor(InsP3R3) in ICC.Protein kinase C(PKC) activator phorbol 12-myristate 13-acetate(PMA) and inhibitor chelerythrine were used to assess the role of PKC in the CCK-8S-evoked [Ca2+]i increment of ICC.RESULTS:ICC were successfully isolated from the gastric antrum of mice and cultured.Cultured ICC were identified by immunofluorescence staining.When given 80 nmol/L or more than 80 nmol/L CCK-8S,the [Ca2+]i in ICC increased and 100 nmol/L CCK-8S significantly increased the mean [Ca2+]i by 59.30% ± 4.85%(P < 0.01).Pretreatment of ICC with 5 μmol/L lorglumide inhibited 100 nmol/L CCK-8S-induced [Ca2+]i increment from 59.30% ± 4.85% to 14.97% ± 9.05%(P < 0.01),suggesting a CCK1R-mediated event.Emptying of intracellular calcium stores by thapsigargin(5 μmol/L) prevented CCK-8S(100 nmol/L) from inducing a [Ca2+]i increase.Moreover,pretreatment with xestospongin C(1 μmol/L) could also abolish the CCK-8S-induced effect,indicating that Ca2+ release from InsP3R-operated stores appeared to be a major mechanism responsible for CCK-8S-induced calcium mobilization in ICC.On the other hand,by removing extracellular calcium or blocking the L-type voltage-operated calcium channel with nifedipine,a smaller but significant rise in the [Ca2+]i could be still elicited by CCK-8S.These data suggest that the [Ca2+]i release is not stimulated or activated by the influx of extracellular Ca2+ in ICC,but the influx of extracellular Ca2+ can facilitate the [Ca2+]i increase evoked by CCK-8S.CCK-8S increased the phosphorylation of InsP3R3,which could be prevented by chelerythrine.Pretreatment with lorglumide(5 μmol/L) could significantly reduce the CCK-8S intensified phosphorylation of InsP3R3.In the positive control group,treatment of cells with PMA also resulted in an enhanced phosphorylation of InsP3R3.Pretreatment with various concentrations of PMA(10 nmol/L-10 μmol/L) apparently inhibited the effect of CCK-8S and the effect of100 nmol/L PMA was most obvious.Likewise,the effect of CCK-8S was augmented by the pretreatment with chelerythrine(10 nmol/L-10 μmol/L) and 100 nmol/L chelerythrine exhibited the maximum effect.CONCLUSION:CCK-8S increases [Ca2+]i in ICC via the CCK1 receptor.This effect depends on the release of InsP3R-operated Ca2+ stores,which is negatively regulated by PKC-mediated phosphorylation of InsP3R3. 展开更多
关键词 Cholecystokinin octapeptide Interstitial cells of Cajal Calcium mobilization Protein kinase C
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Thapsigargin increases apoptotic cell death in human hepatoma BEL-7404 cells
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作者 GU JUN HE LIU +1 位作者 TAO FU YONGHUA XU (Laboratory of Molecular Biology, Naval Medical Research Institute, Shanghai 200433, China)(Laboratory of Cellular and Molecular Oncology, Shang-hai Institute of Cell Biology, Chincse Academy of Sciences, Shanghai 200031 《Cell Research》 SCIE CAS CSCD 1995年第1期59-65,共7页
Effects of thapsigargin, an inhibitor of Ca2+-ATPase in surface of endoplasmic reticulum, on apoptotic cell death were studied in human hepatoma cells of BEL-7404 cell line by using both flow cytometry and electron mi... Effects of thapsigargin, an inhibitor of Ca2+-ATPase in surface of endoplasmic reticulum, on apoptotic cell death were studied in human hepatoma cells of BEL-7404 cell line by using both flow cytometry and electron mi-croscopy Propidium iodide staining and flow cytome- try revealed that in the serum-free condition, thapsigar-gin increased the rate of apoptosis of BEL- 7404 cells in a dose-dependent manner. Prolongation of the period of serum-free condition enhanced the apoptosis induced by thapsigargin treatment. Morphological observation with electron microscope further demonstrated that chromatin condensation and fragmentation, apoptotic bodies existed in TG-treated cells, supporting that thapsigargin is a po-tent activator of apoptosis in the cells. 展开更多
关键词 apoptosis CALCIUM human hepatoma cells THAPSIGARGIN flow cytometry electron microscope
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Design, synthesis and evaluation of novel non-ATP competitive CHK1 inhibitors as chemotherapy sensitizing agents
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作者 李远新 韩子飞 +2 位作者 田超 张志丽 刘俊义 《Journal of Chinese Pharmaceutical Sciences》 CAS CSCD 2016年第10期726-736,共11页
A series of urea-based compounds containing purine moieties were designed and synthesized as novel non-ATP competitive CHK1 inhibitors. The biological evaluation showed that several target compounds exhibited more pot... A series of urea-based compounds containing purine moieties were designed and synthesized as novel non-ATP competitive CHK1 inhibitors. The biological evaluation showed that several target compounds exhibited more potent inhibitory effects against CHK1 than the lead compound. In addition, one particular compound displayed synergistic effects with gemcitabine against HT29 cells. 展开更多
关键词 CHK1 inhibitors Non-atp competitive Anti-cancer synergistic effect
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Allosteric kinase inhibitors:a new paradigm for effective and selective modulation of kinase activities
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作者 杨洪亮 陈婷 +1 位作者 柏旭 裴亚中 《Journal of Chinese Pharmaceutical Sciences》 CAS 2012年第6期531-543,共13页
Dysregulation of kinases has been proven to be one of the main causes of abnormal growth and survival of cancer cells.Selective modulations of kinase activities have become the focus of many research programs for the ... Dysregulation of kinases has been proven to be one of the main causes of abnormal growth and survival of cancer cells.Selective modulations of kinase activities have become the focus of many research programs for the development of safe and effective chemotherapy for cancers.So far,fifteen kinase inhibitors have received FDA approval for the treatment of various forms of cancers.Among them,the allosteric kinase inhibitors have been shown to have superior clinical profile in terms of safety and efficacy.In this review,we summarize the allosteric conformations of kinases,their corresponding inhibitors and the modes of their interactions. 展开更多
关键词 Protein kinase Allosteric conformation DFG-out atp non-competitive Kinase inhibitor
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