首页 > 最新文献

Zhongguo yao li xue bao = Acta pharmacologica Sinica最新文献

英文 中文
Scavenging effect of chinonin on free radicals studied with quantum chemistry. 用量子化学方法研究了甲壳素对自由基的清除作用。
H Y Zhang

Aim: To study whether the xanthonoid structure can enhance the ability of chinonin to scavenge free radicals and to understand the sequence of activity of chinonin hydroxyls.

Methods: Semiempirical quantum chemistry method AM1 was employed to calculate delta HOF values, the differences between heat of formations of mother molecule and its free radicals, and spin density distribution of different states of chinonin. delta HOF values were used as theoretical indices to measure scavenging activity of chinonin on free radicals and effects of structure on delta HOF values were investigated.

Results: delta HOF values of different phenolics were calculated to be 139.09 kJ.mol-1 (O5-H6), 141.46 kJ.mol-1 (O4-H5), 185.14 kJ.mol-1 (O2-H2) and 195.71 kJ.mol-1 (O1-H1). Spin density distribution of free radicals were obtained as well.

Conclusion: Xanthonoid structure of chinonin made ring C to display high passive effect on ring B, which reduced scavenging activity of phenolics of ring B on free radicals. The sequence of activities of chinonin hydroxyls was O5-H6 > O4-H5 > O2-H2 > O1-H1.

目的:研究黄嘌呤类结构是否能增强茶皂素清除自由基的能力,了解茶皂素羟基的活性序列。方法:采用半经验量子化学方法AM1,计算δ HOF值、母分子生成热与自由基生成热之差、不同状态下紫茶苷的自旋密度分布。以δ HOF值作为理论指标,考察了其结构对δ HOF值的影响。结果:不同酚类化合物的δ HOF值为139.09 kJ。mol-1 (O5-H6), 141.46 kJ。mol-1 (O4-H5), 185.14 kJ。mol-1 (O2-H2)和195.71 kJ。mol-1 (O1-H1)。得到了自由基的自旋密度分布。结论:黄嘌呤类结构使C环对B环表现出较高的被动作用,降低了B环中酚类物质对自由基的清除能力。紫茶素各羟基的活性顺序为O5-H6 > O4-H5 > O2-H2 > O1-H1。
{"title":"Scavenging effect of chinonin on free radicals studied with quantum chemistry.","authors":"H Y Zhang","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Aim: </strong>To study whether the xanthonoid structure can enhance the ability of chinonin to scavenge free radicals and to understand the sequence of activity of chinonin hydroxyls.</p><p><strong>Methods: </strong>Semiempirical quantum chemistry method AM1 was employed to calculate delta HOF values, the differences between heat of formations of mother molecule and its free radicals, and spin density distribution of different states of chinonin. delta HOF values were used as theoretical indices to measure scavenging activity of chinonin on free radicals and effects of structure on delta HOF values were investigated.</p><p><strong>Results: </strong>delta HOF values of different phenolics were calculated to be 139.09 kJ.mol-1 (O5-H6), 141.46 kJ.mol-1 (O4-H5), 185.14 kJ.mol-1 (O2-H2) and 195.71 kJ.mol-1 (O1-H1). Spin density distribution of free radicals were obtained as well.</p><p><strong>Conclusion: </strong>Xanthonoid structure of chinonin made ring C to display high passive effect on ring B, which reduced scavenging activity of phenolics of ring B on free radicals. The sequence of activities of chinonin hydroxyls was O5-H6 > O4-H5 > O2-H2 > O1-H1.</p>","PeriodicalId":24002,"journal":{"name":"Zhongguo yao li xue bao = Acta pharmacologica Sinica","volume":"20 6","pages":"555-8"},"PeriodicalIF":0.0,"publicationDate":"1999-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21532724","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Protective effect of melatonin on injuried cerebral neurons is associated with bcl-2 protein over-expression. 褪黑素对脑损伤神经元的保护作用与bcl-2蛋白过表达有关。
X Ling, L M Zhang, S D Lu, X J Li, F Y Sun

Aim: To study the protective effect of melatonin against neuronal injury and the possible roles of alteration in the expression of bcl-2 and bax following brain ischemia.

Methods: Brain ischemia was induced by left middle cerebral artery occlusion (MCAO) for 60 min in rats. Brain damage was evaluated by the infarct area and the neuronal cell counting. The expression of bcl-2 and bax was analyzed by immunohistochemical method.

Results: Melatonin decreased the infarct area and prevented the neuronal death after 24-h reperfusion following 1-h MCAO. Melatonin given before the ischemia enhanced the expression of bcl-2 in the penumbra area and had no significant effect on the expression of bax.

Conclusion: Melatonin effectively attenuated ischemic brain injury and increased the expression of neuronal bcl-2 in the ischemic brain, indicating that the protective effect of melatonin was associated with up-regulation of bcl-2 in ischemia-induced neuronal death.

目的:探讨褪黑素对脑缺血后神经元损伤的保护作用及其对bcl-2和bax表达改变的可能作用。方法:左大脑中动脉闭塞(MCAO)致大鼠脑缺血60 min。通过脑梗死面积和神经元计数评估脑损伤程度。免疫组化法分析bcl-2和bax的表达。结果:褪黑素可减少梗死面积,防止MCAO 1 h后24 h再灌注神经元死亡。缺血前给予褪黑素可增强半影区bcl-2的表达,对bax的表达无明显影响。结论:褪黑素能有效减轻缺血性脑损伤,增加缺血性脑神经元bcl-2的表达,提示褪黑素的保护作用与bcl-2在缺血神经元死亡中的上调有关。
{"title":"Protective effect of melatonin on injuried cerebral neurons is associated with bcl-2 protein over-expression.","authors":"X Ling,&nbsp;L M Zhang,&nbsp;S D Lu,&nbsp;X J Li,&nbsp;F Y Sun","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Aim: </strong>To study the protective effect of melatonin against neuronal injury and the possible roles of alteration in the expression of bcl-2 and bax following brain ischemia.</p><p><strong>Methods: </strong>Brain ischemia was induced by left middle cerebral artery occlusion (MCAO) for 60 min in rats. Brain damage was evaluated by the infarct area and the neuronal cell counting. The expression of bcl-2 and bax was analyzed by immunohistochemical method.</p><p><strong>Results: </strong>Melatonin decreased the infarct area and prevented the neuronal death after 24-h reperfusion following 1-h MCAO. Melatonin given before the ischemia enhanced the expression of bcl-2 in the penumbra area and had no significant effect on the expression of bax.</p><p><strong>Conclusion: </strong>Melatonin effectively attenuated ischemic brain injury and increased the expression of neuronal bcl-2 in the ischemic brain, indicating that the protective effect of melatonin was associated with up-regulation of bcl-2 in ischemia-induced neuronal death.</p>","PeriodicalId":24002,"journal":{"name":"Zhongguo yao li xue bao = Acta pharmacologica Sinica","volume":"20 5","pages":"409-14"},"PeriodicalIF":0.0,"publicationDate":"1999-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21531606","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Circumvention of tumor multidrug resistance by a new annonaceous acetogenin: atemoyacin-B. 一种新的无毒醋酸原atemoyacin-B规避肿瘤多药耐药的研究。
L W Fu, Q C Pan, Y J Liang, H B Huang

Aim: To explore the effect of atemoyacin-B (Ate) on overcoming multidrug resistance (MDR).

Methods: Bullatacin (Bul) was used as a positive control. Cytotoxic effects of Bul and Ate were studied with cell culture of human MDR breast adenocarcinoma cells, MCF-7/Dox and human KBv200 cells, and their parental sensitive cell lines MCF-7 and KB. Cytotoxicity was determined by tetrazolium (MTT) assay. The function of P-glycoprotein (P-gp) was examined by Fura 2-AM assay. Cellular accumulation of doxorubicin (Dox) was determined by fluorescence spectrophotometry. Apoptosis was measured by flow cytometry.

Results: IC50 of Ate for MCF-7/Dox, MCF-7, KBv200, and KB cells were 122, 120, 1.34, and 1.27 nmol.L-1, respectively. IC50 of Bul for MCF-7/Dox, MCF-7, KBv200, and KB cells were 0.60, 0.59, 0.04, and 0.04 nmol.L-1, respectively. The cytotoxicities of Bul and Ate to MDR cells were similar to those to parental sensitive cells. Bul and Ate markedly increased cellular Fura-2 and Dox accumulation in MCF-7/Dox cells, but not in MCF-7 cells. The rates of apoptosis in MDR cells were similar to those in sensitive cells induced by Ate.

Conclusion: There was no cross-resistance of P-gp positive MCF-7/Dox and KBv200 cell lines to Bul and Ate as compared with their sensitive P-gp negative MCF-7 and KB cell lines. The mechanism of the circumvention of MDR was associated with the decrease of P-gp function and the increase of cellular drug accumulation in MDR cells.

目的:探讨atemoyacin-B (Ate)治疗多药耐药(MDR)的作用。方法:以布拉他星(Bul)为阳性对照。通过培养人MDR乳腺腺癌细胞、MCF-7/Dox细胞和人KBv200细胞及其亲本敏感细胞系MCF-7和KB细胞,研究了Bul和Ate的细胞毒作用。四氮唑(MTT)法测定细胞毒性。采用Fura 2-AM法检测p -糖蛋白(P-gp)的功能。用荧光分光光度法测定阿霉素在细胞中的蓄积。流式细胞术检测细胞凋亡。结果:Ate对MCF-7/Dox、MCF-7、KBv200和KB细胞的IC50分别为122、120、1.34和1.27 nmol。l - 1。Bul对MCF-7/Dox、MCF-7、KBv200和KB细胞的IC50分别为0.60、0.59、0.04和0.04 nmol。l - 1。Bul和Ate对MDR细胞的细胞毒性与亲本敏感细胞相似。在MCF-7/Dox细胞中,Bul和Ate显著增加了Fura-2和Dox的积累,而在MCF-7细胞中没有。MDR细胞的凋亡率与Ate诱导的敏感细胞相似。结论:P-gp阳性MCF-7/Dox和KBv200细胞株与P-gp阴性MCF-7和KB细胞株相比,对Bul和Ate无交叉耐药。MDR的规避机制与MDR细胞P-gp功能下降和细胞药物蓄积增加有关。
{"title":"Circumvention of tumor multidrug resistance by a new annonaceous acetogenin: atemoyacin-B.","authors":"L W Fu,&nbsp;Q C Pan,&nbsp;Y J Liang,&nbsp;H B Huang","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Aim: </strong>To explore the effect of atemoyacin-B (Ate) on overcoming multidrug resistance (MDR).</p><p><strong>Methods: </strong>Bullatacin (Bul) was used as a positive control. Cytotoxic effects of Bul and Ate were studied with cell culture of human MDR breast adenocarcinoma cells, MCF-7/Dox and human KBv200 cells, and their parental sensitive cell lines MCF-7 and KB. Cytotoxicity was determined by tetrazolium (MTT) assay. The function of P-glycoprotein (P-gp) was examined by Fura 2-AM assay. Cellular accumulation of doxorubicin (Dox) was determined by fluorescence spectrophotometry. Apoptosis was measured by flow cytometry.</p><p><strong>Results: </strong>IC50 of Ate for MCF-7/Dox, MCF-7, KBv200, and KB cells were 122, 120, 1.34, and 1.27 nmol.L-1, respectively. IC50 of Bul for MCF-7/Dox, MCF-7, KBv200, and KB cells were 0.60, 0.59, 0.04, and 0.04 nmol.L-1, respectively. The cytotoxicities of Bul and Ate to MDR cells were similar to those to parental sensitive cells. Bul and Ate markedly increased cellular Fura-2 and Dox accumulation in MCF-7/Dox cells, but not in MCF-7 cells. The rates of apoptosis in MDR cells were similar to those in sensitive cells induced by Ate.</p><p><strong>Conclusion: </strong>There was no cross-resistance of P-gp positive MCF-7/Dox and KBv200 cell lines to Bul and Ate as compared with their sensitive P-gp negative MCF-7 and KB cell lines. The mechanism of the circumvention of MDR was associated with the decrease of P-gp function and the increase of cellular drug accumulation in MDR cells.</p>","PeriodicalId":24002,"journal":{"name":"Zhongguo yao li xue bao = Acta pharmacologica Sinica","volume":"20 5","pages":"435-9"},"PeriodicalIF":0.0,"publicationDate":"1999-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21532719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Dynamic digital fluorescence ratio imaging of cell calcium in vascular endothelial cells. 血管内皮细胞钙的动态数字荧光比成像。
C Y Kwan, T K Kwan

Aim: To study the spatial and temporal distribution of intracellular Ca2+ concentration in cultured bovine pulmonary artery endothelial (BPAE) cells.

Methods: Cultured BPAE cells were loaded with Fura-2 and observed under an inverted microscope coupled to a microfluorimeter, which enables pixel-to-pixel ratio imaging of the BPAE cells in real time.

Results: Addition of Ca2+ 1-2 mmol.L-1 to BPAE cells, which were exposed to Ca(2+)-free medium containing egtazic acid, resulted in a transient elevation of cytosolic Ca2+ concentration, which rapidly returned to the resting level. Biphasic elevation (a larger transient phase followed by a smaller sustained phase) of intracellular Ca2+ concentration was observed upon the addition of ATP (via activation of surface membrane receptor). 4-Chloro-3-ethyl phenol (CEP; an activator of Ca(2+)-induced Ca2+ channels) potently induced elevation of Ca2+ level. Cyclopiazonic acid (CPA; an inhibitor of endoplasmic reticulum Ca(2+)-ATPase pump) offered a more sustained elevation of Ca2+. In most cases, the highest level of Ca2+ elevation was observed around the cell peripheries, sometimes at rest and particularly upon stimulation. Ca2+ elevation associated with nuclear complex seemed to be higher compared to that in the cytosolic compartment.

Conclusion: Changes of cell Ca2+ upon stimulation by various agents that acted at different intracellular sites were found to be temporarily and spatially heterogenous among BPAE cells. At the single cell level, Ca2+ elevation seemed to occur initially near the peripheral region followed by the nuclear region. This study raised the possibility that nuclear Ca2+ and cytosolic Ca2+ might be regulated independently in BPAE cells.

目的:研究培养的牛肺动脉内皮(BPAE)细胞内Ca2+浓度的时空分布。方法:将培养的BPAE细胞负载Fura-2,在倒置显微镜下与微荧光仪耦合观察,实现BPAE细胞的实时像素比成像。结果:添加Ca2+ 1-2 mmol。L-1至BPAE细胞暴露于含egtaic酸的无Ca(2+)培养基中,导致胞质Ca2+浓度瞬间升高,并迅速恢复到静息水平。在添加ATP(通过激活表面膜受体)后,观察到细胞内Ca2+浓度的双相升高(较大的短暂期随后较小的持续期)。4-氯-3-乙基苯酚;一种Ca(2+)诱导的Ca2+通道的激活剂)能诱导Ca2+水平的升高。环吡唑酸;一种内质网Ca(2+)- atp酶泵抑制剂)提供了更持续的Ca2+升高。在大多数情况下,在细胞周围观察到最高水平的Ca2+升高,有时在休息时,特别是在刺激时。与核复合体相关的Ca2+升高似乎高于细胞质室。结论:在BPAE细胞中,受作用于细胞内不同部位的各种药物的刺激,细胞Ca2+的变化具有暂时性和空间异质性。在单细胞水平,Ca2+升高似乎首先发生在外周区域附近,然后是核区域。本研究提出了核Ca2+和胞质Ca2+可能在BPAE细胞中独立调节的可能性。
{"title":"Dynamic digital fluorescence ratio imaging of cell calcium in vascular endothelial cells.","authors":"C Y Kwan,&nbsp;T K Kwan","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Aim: </strong>To study the spatial and temporal distribution of intracellular Ca2+ concentration in cultured bovine pulmonary artery endothelial (BPAE) cells.</p><p><strong>Methods: </strong>Cultured BPAE cells were loaded with Fura-2 and observed under an inverted microscope coupled to a microfluorimeter, which enables pixel-to-pixel ratio imaging of the BPAE cells in real time.</p><p><strong>Results: </strong>Addition of Ca2+ 1-2 mmol.L-1 to BPAE cells, which were exposed to Ca(2+)-free medium containing egtazic acid, resulted in a transient elevation of cytosolic Ca2+ concentration, which rapidly returned to the resting level. Biphasic elevation (a larger transient phase followed by a smaller sustained phase) of intracellular Ca2+ concentration was observed upon the addition of ATP (via activation of surface membrane receptor). 4-Chloro-3-ethyl phenol (CEP; an activator of Ca(2+)-induced Ca2+ channels) potently induced elevation of Ca2+ level. Cyclopiazonic acid (CPA; an inhibitor of endoplasmic reticulum Ca(2+)-ATPase pump) offered a more sustained elevation of Ca2+. In most cases, the highest level of Ca2+ elevation was observed around the cell peripheries, sometimes at rest and particularly upon stimulation. Ca2+ elevation associated with nuclear complex seemed to be higher compared to that in the cytosolic compartment.</p><p><strong>Conclusion: </strong>Changes of cell Ca2+ upon stimulation by various agents that acted at different intracellular sites were found to be temporarily and spatially heterogenous among BPAE cells. At the single cell level, Ca2+ elevation seemed to occur initially near the peripheral region followed by the nuclear region. This study raised the possibility that nuclear Ca2+ and cytosolic Ca2+ might be regulated independently in BPAE cells.</p>","PeriodicalId":24002,"journal":{"name":"Zhongguo yao li xue bao = Acta pharmacologica Sinica","volume":"20 5","pages":"385-90"},"PeriodicalIF":0.0,"publicationDate":"1999-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21531601","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Antagonistic effects of Ginkgo biloba extract on adhesion of monocytes and neutrophils to cultured cerebral microvascular endothelial cells. 银杏叶提取物对培养的脑微血管内皮细胞粘附单核细胞和中性粒细胞的拮抗作用。
J P Xu, Y C Rui, T J Li

Aim: To study the action of Ginkgo biloba extract (GbE) on tumor necrosis factor (TNF-alpha)-induced adhesion of monocytes (Mon) and neutrophils (Neu) to cultured cerebral microvascular endothelial cells.

Methods: TNF-alpha-induced endothelial adhesivity toward Mon and Neu was studied using bovine cerebral microvascular endothelial cells (BCMEC) in vitro. The number of Mon and Neu adhering to the BCMEC monolayers was determined by flow cytometry.

Results: Pretreatment of BCMEC with TNF-alpha increased Mon and Neu adhesion to BCMEC from 12.5% +/- 0.2% to 31.3% +/- 0.5% and from 13.8% +/- 0.4% to 32.1% +/- 0.5%, respectively. GbE (1-100 mg.L-1) inhibited the effect of TNF-alpha in a concentration-dependent manner. E-selectin mAb (1 mg.L-1) blocked Mon and Neu adhesion to BCMEC induced by TNF-alpha.

Conclusion: The inhibition of GbE on Mon and Neu adhesion to BCMEC was mediated through the suppression of E-selection expression.

目的:研究银杏叶提取物(GbE)对肿瘤坏死因子(tnf - α)诱导的单核细胞(Mon)和中性粒细胞(Neu)对培养的脑微血管内皮细胞粘附的影响。方法:利用体外培养的牛脑微血管内皮细胞(BCMEC),研究tnf α诱导的内皮细胞对Mon和Neu的粘附性。流式细胞术检测Mon和Neu粘附BCMEC单层细胞的数量。结果:tnf - α预处理BCMEC后,Mon和Neu与BCMEC的粘附分别从12.5% +/- 0.2%和13.8% +/- 0.4%增加到31.3% +/- 0.5%和32.1% +/- 0.5%。GbE (1 ~ 100 mg.L-1)对tnf - α的抑制作用呈浓度依赖性。E-selectin mAb (1 mg.L-1)可阻断tnf - α诱导的Mon和new对BCMEC的粘附。结论:GbE通过抑制E-selection的表达来抑制Mon和new对BCMEC的粘附。
{"title":"Antagonistic effects of Ginkgo biloba extract on adhesion of monocytes and neutrophils to cultured cerebral microvascular endothelial cells.","authors":"J P Xu,&nbsp;Y C Rui,&nbsp;T J Li","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Aim: </strong>To study the action of Ginkgo biloba extract (GbE) on tumor necrosis factor (TNF-alpha)-induced adhesion of monocytes (Mon) and neutrophils (Neu) to cultured cerebral microvascular endothelial cells.</p><p><strong>Methods: </strong>TNF-alpha-induced endothelial adhesivity toward Mon and Neu was studied using bovine cerebral microvascular endothelial cells (BCMEC) in vitro. The number of Mon and Neu adhering to the BCMEC monolayers was determined by flow cytometry.</p><p><strong>Results: </strong>Pretreatment of BCMEC with TNF-alpha increased Mon and Neu adhesion to BCMEC from 12.5% +/- 0.2% to 31.3% +/- 0.5% and from 13.8% +/- 0.4% to 32.1% +/- 0.5%, respectively. GbE (1-100 mg.L-1) inhibited the effect of TNF-alpha in a concentration-dependent manner. E-selectin mAb (1 mg.L-1) blocked Mon and Neu adhesion to BCMEC induced by TNF-alpha.</p><p><strong>Conclusion: </strong>The inhibition of GbE on Mon and Neu adhesion to BCMEC was mediated through the suppression of E-selection expression.</p>","PeriodicalId":24002,"journal":{"name":"Zhongguo yao li xue bao = Acta pharmacologica Sinica","volume":"20 5","pages":"423-5"},"PeriodicalIF":0.0,"publicationDate":"1999-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21532716","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Apoptosis and necrosis induced by sulfur mustard in Hela cells. 硫芥诱导Hela细胞凋亡和坏死。
J Sun, Y X Wang, M J Sun

Aim: To study the apoptotic effect of sulfur mustard (SM) on Hela cells.

Methods: Exponentially growing Hela cells were treated with SM at various concentrations for 3 h, then apoptosis was examined by electron-microscope, DNA gel electrophoresis, and flow cytometry.

Results: SM 1 mumol.L-1 arrested cell growth. After treatment with SM 10-100 mumol.L-1, cells were mainly blocked at G1-phase with apoptosis. Agarose gel electrophoresis of DNA from cells treated with SM revealed "DNA Ladder." About 33% of the Hela cells showed apoptosis 12 h after 3-h treatment with SM 100 mumol.L-1 as determined by flow cytometry and the S-phase cells were more susceptible. However, SM 1000 mumol.L-1 caused marked necrosis in Hela cells.

Conclusion: SM caused 2 distinct forms of cell death, apoptosis or necrosis, in Hela cells in a concentration-dependent manner.

目的:研究硫芥(SM)对Hela细胞凋亡的影响。方法:用不同浓度的SM处理指数生长的Hela细胞3 h,用电镜、DNA凝胶电泳、流式细胞术观察细胞凋亡情况。结果:sm1mumol;L-1抑制细胞生长。经SM 10-100 μ mol处理后。L-1时,细胞主要阻滞在g1期并发生凋亡。经SM处理的细胞DNA琼脂糖凝胶电泳显示“DNA阶梯”。sm100 mumol作用3 h后12 h,约33%的Hela细胞出现凋亡。流式细胞术检测的L-1和s期细胞更敏感。然而,sm1000 μ mol。L-1引起Hela细胞明显坏死。结论:SM可引起Hela细胞凋亡和坏死两种不同形式的细胞死亡,并呈浓度依赖性。
{"title":"Apoptosis and necrosis induced by sulfur mustard in Hela cells.","authors":"J Sun,&nbsp;Y X Wang,&nbsp;M J Sun","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Aim: </strong>To study the apoptotic effect of sulfur mustard (SM) on Hela cells.</p><p><strong>Methods: </strong>Exponentially growing Hela cells were treated with SM at various concentrations for 3 h, then apoptosis was examined by electron-microscope, DNA gel electrophoresis, and flow cytometry.</p><p><strong>Results: </strong>SM 1 mumol.L-1 arrested cell growth. After treatment with SM 10-100 mumol.L-1, cells were mainly blocked at G1-phase with apoptosis. Agarose gel electrophoresis of DNA from cells treated with SM revealed \"DNA Ladder.\" About 33% of the Hela cells showed apoptosis 12 h after 3-h treatment with SM 100 mumol.L-1 as determined by flow cytometry and the S-phase cells were more susceptible. However, SM 1000 mumol.L-1 caused marked necrosis in Hela cells.</p><p><strong>Conclusion: </strong>SM caused 2 distinct forms of cell death, apoptosis or necrosis, in Hela cells in a concentration-dependent manner.</p>","PeriodicalId":24002,"journal":{"name":"Zhongguo yao li xue bao = Acta pharmacologica Sinica","volume":"20 5","pages":"445-8"},"PeriodicalIF":0.0,"publicationDate":"1999-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21532722","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
6,7-dimethoxycoumarin attenuated cisplatin-induced DNA interstrand crosslink and DNA-protein crosslink in primary cultured rabbit kidney proximal tubular cells. 6,7-二甲氧基香豆素减弱顺铂诱导的兔肾近端小管细胞DNA链间交联和DNA-蛋白交联。
S J Liu, S W Zhou

Aim: To study the mechanism of cisplatin interaction with DNA, and the attenuating effects of 6,7-dimethoxycoumarin (DMOC) on crosslink.

Methods: Primary cultured rabbit kidney proximal tubular cells (PTC) were established. DNA interstrand crosslink was assayed with ethidium bromide binding and DNA-protein crosslink with 125I-postlabelling. PTC were incubated with cisplatin for 24 h. DMOC was preincubated with PTC for 24 h, and cisplatin (26 mumol.L-1) was added into culture and incubated for another 24 h.

Results: Cisplatin induced formation of DNA interstrand crosslink (13, 26, 52, and 78 mumol.L-1) and DNA-protein crosslink (26, 52, and 78 mumol.L-1) (P < 0.01). DNA interstrand crosslink in DMOC (0.4, 4, and 8 mg.L-1) and DNA-protein crosslink in DMOC (4, 8 mg.L-1) were less than those in cisplatin group (26 mumol.L-1), respectively (P < 0.01).

Conclusion: The mechanisms of cisplatin interaction with DNA in PTC were DNA interstrand crosslink and DNA-protein crosslink, and DMOC attenuated these effects in vitro.

目的:研究顺铂与DNA相互作用的机制,以及6,7-二甲氧基香豆素(DMOC)对交联的减弱作用。方法:建立原代培养兔肾近端小管细胞(PTC)。采用溴化乙啶结合法测定DNA链间交联,采用125i后标记法测定DNA-蛋白交联。PTC与顺铂共孵育24 h, DMOC与PTC共预孵育24 h,加入顺铂(26、26、52、78 mumol.L-1)再孵育24 h。结果:顺铂诱导DNA链间交联(13、26、52、78 mumol.L-1)和DNA-蛋白交联(26、52、78 mumol.L-1)的形成(P < 0.01)。DMOC组(0.4、4、8 mg.L-1) DNA链间交联和DMOC组(4、8 mg.L-1) DNA-蛋白交联均低于顺铂组(26 mmol . l -1) (P < 0.01)。结论:顺铂在PTC中与DNA的相互作用机制为DNA链间交联和DNA-蛋白交联,DMOC在体外可减弱这两种作用。
{"title":"6,7-dimethoxycoumarin attenuated cisplatin-induced DNA interstrand crosslink and DNA-protein crosslink in primary cultured rabbit kidney proximal tubular cells.","authors":"S J Liu,&nbsp;S W Zhou","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Aim: </strong>To study the mechanism of cisplatin interaction with DNA, and the attenuating effects of 6,7-dimethoxycoumarin (DMOC) on crosslink.</p><p><strong>Methods: </strong>Primary cultured rabbit kidney proximal tubular cells (PTC) were established. DNA interstrand crosslink was assayed with ethidium bromide binding and DNA-protein crosslink with 125I-postlabelling. PTC were incubated with cisplatin for 24 h. DMOC was preincubated with PTC for 24 h, and cisplatin (26 mumol.L-1) was added into culture and incubated for another 24 h.</p><p><strong>Results: </strong>Cisplatin induced formation of DNA interstrand crosslink (13, 26, 52, and 78 mumol.L-1) and DNA-protein crosslink (26, 52, and 78 mumol.L-1) (P < 0.01). DNA interstrand crosslink in DMOC (0.4, 4, and 8 mg.L-1) and DNA-protein crosslink in DMOC (4, 8 mg.L-1) were less than those in cisplatin group (26 mumol.L-1), respectively (P < 0.01).</p><p><strong>Conclusion: </strong>The mechanisms of cisplatin interaction with DNA in PTC were DNA interstrand crosslink and DNA-protein crosslink, and DMOC attenuated these effects in vitro.</p>","PeriodicalId":24002,"journal":{"name":"Zhongguo yao li xue bao = Acta pharmacologica Sinica","volume":"20 5","pages":"391-4"},"PeriodicalIF":0.0,"publicationDate":"1999-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21531602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Quercetin decreased heart rate and cardiomyocyte Ca2+ oscillation frequency in rats and prevented cardiac hypertrophy in mice. 槲皮素降低大鼠心率和心肌细胞Ca2+振荡频率,防止小鼠心肌肥厚。
Y Wang, H Y Wang, Z K Yuan, X N Zhao, J X Wang, Z X Zhang

Aim: To study the effects of quercetin (Que) on myocardial excitation-contraction coupling and cardiac remodeling.

Methods: Left ventricles and femoral arteries of rats were cannulated for hemodynamic recording. Mouse cardiac hypertrophy was induced by abdominal aortic coarctation (AAC). Cultured myocardial cells in neonatal rats were loaded with Fura 2-AM. The intracellular calcium ([Ca2+]i) and spontaneous [Ca2+]i oscillations ([Ca2+]i-SO) were tested by AR-CM-MIC cation measurement system.

Results: Que 3 or 25 mg.kg-1 i.v. in rats decreased heart rate from (420 +/- 19) to (390 +/- 15) and (314 +/- 18) beat.min-1, respectively, companied with very modest changes in both left ventricular pressures (LVP) and its differential dpLV/dtmax. Que 10, 50, 250 mumol.L-1 concentration-dependently slowed the frequency of [Ca2+]i-SO in cultured myocardial cells from (26 +/- 4) to (25 +/- 3), (18 +/- 4), and (12 +/- 3) time.min-1, respectively, but did not change their resting [Ca2+]i or amplitudes of [Ca2+]i-SO. Similarly, the increases in frequency of [Ca2+]i-SO caused by either isoproterenol (Iso) or ouabain (Oua) were prevented by Que 100 mumol.L-1, while the simultaneous increases in amplitude of [Ca2+]i-SO remained. Besides, [Ca2+]i rises excited by angiotensin II (Ang II) but not high [K+]o were prevented by Que 100 mumol.L-1. Daily administration of Que 120 mg.kg-1 i.g. for 5 d markedly prevented the cardiac hypertrophy in AAC mice, without effects on the ventricular mass to body weight ratio (VM/BW) in sham-operated mice.

Conclusion: Que decreased myocardial [Ca2+]i-oscillation frequency and prevented cardiac remodeling, but had no direct effect on cardiac excitation-contraction coupling.

目的:研究槲皮素对心肌兴奋-收缩耦合及心脏重构的影响。方法:取大鼠左心室和股动脉插管进行血流动力学记录。腹腔主动脉缩窄(AAC)诱导小鼠心肌肥厚。培养的新生大鼠心肌细胞加载Fura 2-AM。采用AR-CM-MIC阳离子测量系统检测细胞内钙离子([Ca2+]i)和自发[Ca2+]i振荡([Ca2+]i- so)。结果:Que 3或25mg。Kg-1静脉滴注使大鼠心率从(420 +/- 19)降至(390 +/- 15)和(314 +/- 18)次。min-1分别伴有左室压(LVP)及其差值dpLV/dtmax的非常温和的变化。Que 10,50,250 mumol。L-1浓度依赖性地减慢了培养心肌细胞中[Ca2+]i-SO的频率,从(26 +/- 4)到(25 +/- 3)、(18 +/- 4)和(12 +/- 3)时间。但不改变其静息[Ca2+]i或[Ca2+]i- so的振幅。同样,由异丙肾上腺素(Iso)或瓦阿因(Oua)引起的[Ca2+]i-SO频率的增加可以通过Que 100 mumol来预防。L-1,而[Ca2+]i-SO的幅度同时增加。此外,Que 100 mol. l -1能抑制血管紧张素II (Ang II)引起的[Ca2+]i升高,但不能抑制高[K+]o升高。每日给药Que 120 mg。kg-1 ig 5 d可明显预防AAC小鼠心肌肥厚,对假手术小鼠心室质量与体重比(VM/BW)无影响。结论:茴香可降低心肌[Ca2+]i振荡频率,防止心肌重构,但对心脏兴奋-收缩耦合无直接影响。
{"title":"Quercetin decreased heart rate and cardiomyocyte Ca2+ oscillation frequency in rats and prevented cardiac hypertrophy in mice.","authors":"Y Wang,&nbsp;H Y Wang,&nbsp;Z K Yuan,&nbsp;X N Zhao,&nbsp;J X Wang,&nbsp;Z X Zhang","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Aim: </strong>To study the effects of quercetin (Que) on myocardial excitation-contraction coupling and cardiac remodeling.</p><p><strong>Methods: </strong>Left ventricles and femoral arteries of rats were cannulated for hemodynamic recording. Mouse cardiac hypertrophy was induced by abdominal aortic coarctation (AAC). Cultured myocardial cells in neonatal rats were loaded with Fura 2-AM. The intracellular calcium ([Ca2+]i) and spontaneous [Ca2+]i oscillations ([Ca2+]i-SO) were tested by AR-CM-MIC cation measurement system.</p><p><strong>Results: </strong>Que 3 or 25 mg.kg-1 i.v. in rats decreased heart rate from (420 +/- 19) to (390 +/- 15) and (314 +/- 18) beat.min-1, respectively, companied with very modest changes in both left ventricular pressures (LVP) and its differential dpLV/dtmax. Que 10, 50, 250 mumol.L-1 concentration-dependently slowed the frequency of [Ca2+]i-SO in cultured myocardial cells from (26 +/- 4) to (25 +/- 3), (18 +/- 4), and (12 +/- 3) time.min-1, respectively, but did not change their resting [Ca2+]i or amplitudes of [Ca2+]i-SO. Similarly, the increases in frequency of [Ca2+]i-SO caused by either isoproterenol (Iso) or ouabain (Oua) were prevented by Que 100 mumol.L-1, while the simultaneous increases in amplitude of [Ca2+]i-SO remained. Besides, [Ca2+]i rises excited by angiotensin II (Ang II) but not high [K+]o were prevented by Que 100 mumol.L-1. Daily administration of Que 120 mg.kg-1 i.g. for 5 d markedly prevented the cardiac hypertrophy in AAC mice, without effects on the ventricular mass to body weight ratio (VM/BW) in sham-operated mice.</p><p><strong>Conclusion: </strong>Que decreased myocardial [Ca2+]i-oscillation frequency and prevented cardiac remodeling, but had no direct effect on cardiac excitation-contraction coupling.</p>","PeriodicalId":24002,"journal":{"name":"Zhongguo yao li xue bao = Acta pharmacologica Sinica","volume":"20 5","pages":"426-30"},"PeriodicalIF":0.0,"publicationDate":"1999-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21532717","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Gene therapy for human hepatocellular carcinoma with cytosine deaminase gene and prodrug flucytosine. 胞嘧啶脱氨酶基因与前药氟胞嘧啶治疗人肝癌的研究。
H Z Lü, D Z Wu, Y L Wan, B Gu, H Z Gao, Y Q Liang, J X Wang

Aim: To investigate the antitumor effects of cytosine deaminase (CD) gene in combination with prodrug flucytosine (Flu, 5-fluorocytosine) on human hepatocellular carcinoma.

Methods: CD gene was transduced into human hepatocellular carcinoma cell line SMMC7721 with retroviral method and the cytotoxicity of Flu on the tumor cells was assayed in vitro with clonogenic techniques. The xenograft tumor model in nude mice was used to study in vivo therapeutic effects of CD gene/Flu system against human hepatocellular carcinoma.

Results: CD gene/Flu system had significant antitumor activities on human hepatocellular carcinoma cells in vitro and in nude mice. The antitumor activities of Flu 500 mg.kg-1 on hepatocellular carcinoma xenografts in nude mice were more potent than those of 5-fluouracil 10 mg.kg-1. CD gene/Flu system possessed bystander killing effects on hepatocellular carcinoma xenografts in nude mice.

Conclusion: The experiment demonstrates the potential value of the CD gene/Flu system in the treatment of human hepatocellular carcinoma.

目的:探讨胞嘧啶脱氨酶(CD)基因联合前药氟胞嘧啶(Flu, 5-氟胞嘧啶)对人肝癌的抗肿瘤作用。方法:用逆转录病毒法将CD基因转染人肝癌细胞系SMMC7721,用克隆技术测定流感病毒对肿瘤细胞的体外毒性。采用裸鼠异种移植瘤模型,研究CD基因/流感系统对人肝癌的体内治疗作用。结果:CD基因/流感系统对人肝癌细胞有明显的体外和裸鼠抗肿瘤活性。流感500毫克的抗肿瘤活性。Kg-1对裸鼠肝癌移植瘤的抑制作用强于5-氟尿嘧啶10 mg.kg-1。CD基因/流感系统对裸鼠肝癌移植具有旁观者杀伤作用。结论:本实验证明了CD基因/Flu系统在治疗人肝癌中的潜在价值。
{"title":"Gene therapy for human hepatocellular carcinoma with cytosine deaminase gene and prodrug flucytosine.","authors":"H Z Lü,&nbsp;D Z Wu,&nbsp;Y L Wan,&nbsp;B Gu,&nbsp;H Z Gao,&nbsp;Y Q Liang,&nbsp;J X Wang","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Aim: </strong>To investigate the antitumor effects of cytosine deaminase (CD) gene in combination with prodrug flucytosine (Flu, 5-fluorocytosine) on human hepatocellular carcinoma.</p><p><strong>Methods: </strong>CD gene was transduced into human hepatocellular carcinoma cell line SMMC7721 with retroviral method and the cytotoxicity of Flu on the tumor cells was assayed in vitro with clonogenic techniques. The xenograft tumor model in nude mice was used to study in vivo therapeutic effects of CD gene/Flu system against human hepatocellular carcinoma.</p><p><strong>Results: </strong>CD gene/Flu system had significant antitumor activities on human hepatocellular carcinoma cells in vitro and in nude mice. The antitumor activities of Flu 500 mg.kg-1 on hepatocellular carcinoma xenografts in nude mice were more potent than those of 5-fluouracil 10 mg.kg-1. CD gene/Flu system possessed bystander killing effects on hepatocellular carcinoma xenografts in nude mice.</p><p><strong>Conclusion: </strong>The experiment demonstrates the potential value of the CD gene/Flu system in the treatment of human hepatocellular carcinoma.</p>","PeriodicalId":24002,"journal":{"name":"Zhongguo yao li xue bao = Acta pharmacologica Sinica","volume":"20 5","pages":"440-4"},"PeriodicalIF":0.0,"publicationDate":"1999-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21532720","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Ro 31-8220 inhibits release of interleukin-1 and interleukin-6 from mouse peritoneal macrophages induced by fibrin fibrinogen degradation products. Ro 31-8220抑制纤维蛋白原降解产物诱导的小鼠腹腔巨噬细胞释放白细胞介素-1和白细胞介素-6。
B Zhou, J P Zhang, Z L Hu, Y X Tan, D H Qian

Aim: To study the effect of fibrin fibrinogen degradation products (FFDP) on release of interleukin-1 (IL-1) and interleukin-6 (IL-6) from mouse peritoneal macrophages, and the effect of a new selectively potent protein kinase C inhibitor Ro 31-8220 (Ro).

Methods: IL-1 and IL-6 activities were measured by thymocyte proliferation assay and B9 cell proliferation methyl thiazolyl tetrazolium (MTT) colorimetric method, respectively.

Results: Ro 0.01-1 mumol.L-1 obviously inhibited FFDP-induced release of IL-1 and IL-6 from mouse peritoneal macrophages.

Conclusion: Ro exerted inhibitory effects on FFDP-induced release of IL-1 and IL-6 in vitro.

目的:研究纤维蛋白纤维蛋白原降解产物(FFDP)对小鼠腹腔巨噬细胞中白细胞介素-1 (IL-1)和白细胞介素-6 (IL-6)释放的影响,以及一种新的选择性强效蛋白激酶C抑制剂Ro 31-8220 (Ro)的作用。方法:分别采用胸腺细胞增殖法和B9细胞增殖甲基噻唑四氮唑(MTT)比色法测定白细胞介素-1和白细胞介素-6的活性。结果:Ro 0.01-1 μ mol。L-1明显抑制ffdp诱导的小鼠腹腔巨噬细胞IL-1和IL-6的释放。结论:Ro对ffdp诱导的IL-1和IL-6的体外释放有抑制作用。
{"title":"Ro 31-8220 inhibits release of interleukin-1 and interleukin-6 from mouse peritoneal macrophages induced by fibrin fibrinogen degradation products.","authors":"B Zhou,&nbsp;J P Zhang,&nbsp;Z L Hu,&nbsp;Y X Tan,&nbsp;D H Qian","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Aim: </strong>To study the effect of fibrin fibrinogen degradation products (FFDP) on release of interleukin-1 (IL-1) and interleukin-6 (IL-6) from mouse peritoneal macrophages, and the effect of a new selectively potent protein kinase C inhibitor Ro 31-8220 (Ro).</p><p><strong>Methods: </strong>IL-1 and IL-6 activities were measured by thymocyte proliferation assay and B9 cell proliferation methyl thiazolyl tetrazolium (MTT) colorimetric method, respectively.</p><p><strong>Results: </strong>Ro 0.01-1 mumol.L-1 obviously inhibited FFDP-induced release of IL-1 and IL-6 from mouse peritoneal macrophages.</p><p><strong>Conclusion: </strong>Ro exerted inhibitory effects on FFDP-induced release of IL-1 and IL-6 in vitro.</p>","PeriodicalId":24002,"journal":{"name":"Zhongguo yao li xue bao = Acta pharmacologica Sinica","volume":"20 5","pages":"449-51"},"PeriodicalIF":0.0,"publicationDate":"1999-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21532721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
期刊
Zhongguo yao li xue bao = Acta pharmacologica Sinica
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1