HPMC在盐酸二苯美仑片中的应用

ＨＰＭＣ在盐酸二苯美仑片中的应用谢安云，邓君芳（湖南医药工业研究所，长沙４１００１４）ＡＰＰＬＩＣＡＴＩＯＮＯＦＨＰＭＣＩＮＢＩＦＥＭＥＬＡＮＥＨＹＤＲＯＣＨＬＯＲＩＤＥＴＡＢＬＥＴＳ￥ＸＩＥＡｎ－Ｙｕｎ；ＤＥＮＧＪｕｎ－Ｆａｎｇ（ＨｕｎａｎＩｎｓｔ...     

Effects of tanshinone Ⅱ-A sullfonate on adhesion molecule expression of endothelial cells and platelets in vitro

探讨丹参酮ⅡＡ磺酸钠（Ｔａｎ）对培养人脐静脉内皮细胞（ＨＵＶＥＣ）和人血小板表达粘附分子的影响．方法：用流动血细胞计数仪测定肿瘤坏死因子（ＴＮＦα）诱导人脐静脉内皮细胞ＩＣＡＭ１和凝血酶诱导人血小板Ｐ选择素的表达．结果：ＨＵＶＥＣ经ＴＮＦα处理后，明显增加细胞表面ＩＣＡＭ１的表达，增加ＨＬ６０细胞粘附到内皮细胞表面达加入细胞总数的３０％±６％（对照组为４６％±０７％）．在ＴＮＦα处理前，用Ｔａｎ（２５－２００μｍｏｌ·Ｌ－１）与ＨＵＶＥＣ共孵育，则Ｔａｎ剂量依赖性地抑制ＴＮＦα的作用．Ｔａｎ（２５－２００μｍｏｌ·Ｌ－１）与人血小板孵育后，可剂量依赖性地抑制凝血酶诱导人血小板表面Ｐｓｅｌｅｃｔｉｎ的表达．结论：Ｔａｎ可抑制内皮细胞和血小板表达粘附分子．     

烟碱对白细胞介素1β诱导的培养牛脑微血管内皮细胞表达E-选择素的增强作用

目的··：观察烟碱对牛脑微血管内皮细胞（ＢＣＭＥＣ）表达Ｅ－选择素的影响。方法··：离体培养新生牛脑微血管内皮细胞;血细胞计数仪测定ＢＣＭＥＣ粘附大鼠血单核细胞（ＭＮ）的数目;应用ＥＬＩＳＡ法检测ＢＣＭＥＣ表达Ｅ－选择素的量。结果··：高浓度烟碱（１０－５ｍｏｌ·Ｌ－１）单独作用于ＢＣＭＥＣ２ｈ后,使ＢＣＭＥＣ对ＭＮ的粘附率从１２．９％±ｓ０．４％增至１５．７％±ｓ０．６％,且ＢＣＭＥＣ也可表达少量的Ｅ－选择素;而当烟碱与ＢＣＭＥＣ作用２ｈ后,再经白细胞介素１β（ＩＬ－１β）诱导４ｈ,烟碱可浓度依赖性（１０－７ｍｏｌ·Ｌ－１－１０－５ｍｏｌ·Ｌ－１）地增强ＩＬ－１β的诱导作用,增加ＢＣＭＥＣ对ＭＮ的粘附率以及Ｅ－选择素的表达量;抗Ｅ－选择素单克隆（ＡＥｍＡｂ）能显著阻断ＩＬ－１β诱导ＢＣＭＥＣ后对ＭＮ的粘附率。结论··：烟碱增强ＩＬ－１β诱导的脑微血管内皮细胞表达Ｅ－选择素的作用。     

前列腺素中间体－顺－6－氯－7－羧基二环［2．2．1］庚－3－酮的拆分

前列腺素中间体－顺－６－氯－７－羧基二环［２．２．１］庚－３－酮的拆分陈敏华，游开铭（上海五洲药厂，上海２０００５２）ＲＥＳＯＬＵＴＩＯＮＯＦｃｉｓ－６－ＣＨＬＯＲＯ－７－ＣＡＲＢＯＸＹＢＩＣＹＣＬＯ［２．２．１］ＨＥＰＴＡＮ－３－ＯＮＥＦＯＲＰＲＯ...     

薄膜材料HPMC在庆大霉素片包衣中的应用

薄膜材料ＨＰＭＣ在庆大霉素片包衣中的应用周大熙，程玉玺，蔡艳芬（利群制药厂，山西大同０３７００５）ＡＰＰＬＩＣＡＴＩＯＮＯＦＨＰＭＣＩＮＣＯＡＴＩＮＧＯＦＧＥＮＴＡＭＹＣＩＮＴＡＢＬＥＴＳ￥ＺＨＯＵＤａ－Ｘｉ；ＣＨＥＮＧＹｕ－Ｘｉ；ＣＡＩＹａｎ－Ｆｅ...     

NBS氧化制备熊去氧胆酸中间体7－氧代石胆酸

ＮＢＳ氧化制备熊去氧胆酸中间体７－氧代石胆酸张国明，余晓岚，严崇萍（上海市中药研究所，上海２００１２７）ＩＭＰＲＯＶＥＤＰＲＥＰＥＲＡＴＩＯＮＯＦ７－ＯＸＯＬＩＴＨＯＣＨＯＬＩＣＡＣＩＤ￥ＺＨＡＮＧＧｕｏ－Ｍｉｎｇ；ＹＵＸｉａｏ－Ｌａｎ；ＹＡＮＣｈｏ...     

新的酚嗪类抗生素SHISEN—1的研究：Ⅱ.理化性质及结构鉴定

在筛选ＭＲＳＡ抑制剂的过程中，从稀有放线菌Ｓｔｒｅｐｔｏｐｌａｎｏｓｐｏｒａ ｖｉｒｉｄｉｓ的次级代谢产物中，得到活性化合物ＳＨＩＳＥＮ－１，该化合物为黄色粉末，于２５４及３６４ｎｍ处有最大的紫外吸收峰，经理化性质和光谱分析（ＩＲ、ＵＶ、ＦＡＢ－ＭＳ、ＥＩ－ＭＳ、＾１Ｈ－ＮＭＲ、＾１３Ｃ－ＮＭＲ、ＤＥＰＴ、ＨＭＱＣ、ＨＭＢＣ、＾１Ｈ－＾１Ｈ ＣＯＳＹ），得知它为一个新的酚嗪类抗生素，分子式为Ｃ２２     

Inhibitory effects of α-methyl-4-(3-oxo-2H-1,2-benzoisoselenazol-2-yl)benzeneacetic acid on Cu~(2+) and Fe~(2+) induced oxidative modification of human low density lipoprotein

为观察α－甲基－４－（３－氧－２Ｈ－１，２－苯并异硒唑－２－基）苯乙酸（ＭＢＢＡ）对Ｃｕ２＋及Ｆｅ２＋氧化修饰低密度脂蛋白（ＬＤＬ）的保护作用及其作用机理，采用分光光度法测定ＬＤＬ中丙二醛（ＭＤＡ）和共轭双烯（ＣＤ）的产生量．ＭＢＢＡ（０．２－２μｍｏｌ·Ｌ－１）能以剂量依赖性抑制Ｃｕ２＋及Ｆｅ２＋诱导的ＭＤＡ和ＣＤ生成．２μｍｏｌ·Ｌ－１的ＭＢＢＡ对Ｃｕ２＋诱导ＬＤＬ产生ＭＤＡ和ＣＤ的抑制率分别为８９．７％和６０．３％．０．５ｍｍｏｌ·Ｌ－１ＧＳＨ对ＬＤＬ产生ＭＤＡ无影响，但能显著增强ＭＢＢＡ对ＭＤＡ生成的抑制作用．上述结果表明ＭＢＢＡ对ＬＤＬ氧化修饰的抑制作用可能依赖于其ＧＳＨ－Ｐｘ样活性的作用和（或）直接还原脂质氢过氧化物的作用．     

Detection of DNA damage in peripheral lymphocytes by 7 compounds using comet assay

目的：检测过氧化氢（Ｈ２Ｏ２）、甲磺酸乙酯（ＥＭＳ）、丝裂霉素Ｃ（ＭＭＣ）、二甲基亚硝胺（ＤＭＮＡ）、苯并（ａ）芘（ＢａＰ）、２氨基芴（２ＡＦ）和环磷酰胺（ＣＰ）诱发小鼠、大鼠及人外周血淋巴细胞ＤＮＡ单链断裂．方法：体外单细胞微量凝胶碱性电泳试验（慧星试验）．结果：除ＥＭＳ０９７ｍｍｏｌ·Ｌ－１在小鼠淋巴细胞，ＭＭＣ３０μｍｏｌ·Ｌ－１在小鼠、人淋巴细胞中呈阴性外，其余均为阳性．最低可检测浓度分别为Ｈ２Ｏ２１μｍｏｌ·Ｌ－１，ＥＭＳ０４８ｍｍｏｌ·Ｌ－１，ＢａＰ５０μｍｏｌ·Ｌ－１，ＣＰ２０ｍｍｏｌ·Ｌ－１，ＭＭＣ１０μｍｏｌ·Ｌ－１，ＤＭＮＡ２７３ｍｍｏｌ·Ｌ－１，２ＡＦ６２５μｍｏｌ·Ｌ－１．ＣＰ、ＢａＰ、２ＡＦ需经Ｓ９Ｍｉｘ代谢活化才显示毒性．结论：彗星试验检测出ＭＭＣ诱导大鼠，ＥＭＳ诱导大鼠和人，以及Ｈ２Ｏ２、ＤＭＮＡ、ＢａＰ、ＣＰ和２ＡＦ诱导小鼠、大鼠和人外周血淋巴细胞ＤＮＡ单链断裂损伤．     

普罗布考合成路线图解

普罗布考合成路线图解刘秀杰，沈建民，王松青（沈阳药学院，辽宁１１００１５）ＧＲＡＰＨＩＣＡＬＳＹＮＴＨＥＴＩＣＲＯＵＴＥＳＯＦＰＲＯＢＵＣＯＬ￥ＬＩＵＸｉｕ－Ｊｉｅ；ＳＨＥＮＪｉａｎ－Ｍｉｎ；ＷＡＮＧＳｏｎｇ－Ｑｉｎｇ（ＳｈｅｎｙａｎｇＣｏｌｌｅｇｅ...     

降钙素基因相关肽预适应对溶血磷脂酰胆碱抑制内皮依赖性舒张的…

目的：研究降钙素基因相关肽（ＣＧＲＰ）诱导预适应对溶血磷脂酰胆碱（Ｌｙｓ）抑制内皮依赖性舒张的作用。方法：用苯福林收缩兔与大鼠离体胸主动脉环，观察Ｌｙｓ对乙酰胆碱（ＡＣｈ）所致内皮依赖性舒张的影响。结果：ＣＧＲＰ预处理兔和大鼠离体胸主动脉环显著减轻Ｌｙｓ对ＡＣｈ舒血管效应的抑制，其作用可被蛋白激酶Ｃ（ＰＫＣ）抑制剂Ｈ－７所取消。结论：ＣＧＲＰ诱导预适应对所致内皮细胞损伤具有拮抗作用，此作用与激活Ｐ     

雌二醇抑制豚鼠心室肌细胞内向整流和延迟整流钾通道电流

研究雌二醇对心室肌细胞动作电位,内向整流钾通道电流及延迟整流钾通道电流的影响。方法：全细胞膜片箝技术。结果：ＥＳＴ１０μｍｏｌ．Ｌ＾－１使豚鼠心室肌细胞ＡＰ时程明显缩短,ＡＰＤ５０由给药前（４７４±７１）ｍｓ缩短至（３３０±７５）ｍｓ（Ｐ〈０．０５）,Ｅｓｔ１００μｍｏｌ．Ｌ＾－１使ＡＰＤ５０缩短至（２２９±６７）ｍｓ,ＡＰＤ９０由（５８７±６０）ｍｓ缩短至（４１８±７９）ｍｓ,Ｅｓｔ浓度依赖性地     

1—（2，6—二甲基苯氧基）—2—（3，4—二甲氧基苯乙氨基）丙烷盐酸盐抑制豚鼠心室肌细胞内向整流和延迟整流钾电流

目的:研究1-(2,6-二甲基苯氧基)-2-(3,4-二甲氧基苯乙氨基)丙烷盐酸盐(DDPH)对心室肌细胞动作电位(AP)、内向整流钾通道电流(I_(K1))及延迟整流钾通道电流(I_K)的影响。方法:全细胞膜片箝技术。结果:DDPH 10,100μmol·L~(-1)使豚鼠心室肌细胞AP时程APD_(50)明显缩短;但DDPH(>1μmol·L~(-1))延长APD_(90)。DDPH浓度依赖性地抑制I_K尾电流(I_(K·tail)),EC_(50)为13.3(11.6.6-16.7)μmol·L~(-1)。DDPH(>1.0μmol·L~(-1))明显抑制I_(Kl);同时,DDPH使I_(Kl)翻转电位向正电位方向移动。结论:DDPH对豚鼠心室肌细胞I_(Kl)和I_K具有明显的抑制作用。     

槲皮素单硫酸酯钠盐对凝血酶诱导的猪血小板聚集的抑制作用

研究槲皮素单硫酸酯钠盐对凝血酶诱导的猪血小板聚集的抑制作用。方法：用比浊法测定血小板聚集,Ｆｕｒａ ２－ＡＭ荧光法检测胞浆游离钙浓度（「Ｃａ＾２＋）ｉ」。用组蛋白ⅢＳ,「γ＾３２Ｐ」ＡＴＰ与蛋白激酶Ｃ酶液一起温育的方法测定ＰＫＣ的活性。用ＳＤＳ－ＰＡＧＥ分离骨架蛋白。     

延髓腹外侧头端注射莫索尼定对大鼠血压,心率和肾交感神经放电…

目的：观察延髓腹外侧头端（ＲＶＬＭ）注射莫索尼定（Ｍｏｘ）对麻醉大鼠血压（ＢＰ）、心率（ＨＲ）及肾交感神经放电（ＲＳＮＡ）的影响。方法：麻醉大鼠ＲＶＬＭ注射１μＬ Ｍｏｘ１，１０，１００μｍｏｌ·Ｌ＾－１，同步记录ＢＰ，ＨＲ及ＲＳＮＡ。结果：Ｍｏｘ１，１０，１００μｍｏｌ·Ｌ＾－１分别使ＢＰ从１３．９±１．０ｋＰａ降至１３．０±１．７ｋＰａ（Ｐ〈０．０５），１３．８±１．８ｋＰａ至１１．４±１．５     

Inhibitory effects of dauricine on potassium currents in guinea pig ventricular myocytes

AIM: To study the effects of dauricine(Dau) on the rapidly activating component (IKr), the slowly activating component (IKs) of the delayed rectifier potassium current, and the inward rectifier potassium current (IKl) in guinea pig ventricular myocytes. METHODS: Single myocytes were dissociated by enzymatic dissociation method. The currents were recorded with the whole-cell configuration of the patch-clamp technique. RESULTS: (1) Dau 1, 3, 10, 30, and 100 mumol.L-1 blocked IKr and tail current (IKr-tail) in a concentration-dependent manner. The IC50 for block of IKr-tail was 16 (95% confidence limits: 13-22) mumol.L-1. The time constant of IKr-tail deactivation was (140 +/- 38) ms in the control and (130 +/- 26) ms in the presence of Dau 30 mumol.L-1 (n = 6 cells from 3 animals, P > 0.05). (2) Dau 1-100 mumol.L-1 produced concentration-dependent blocks of IKs and tail current (IKs-tail). The IC50 value for block of IKs-tail was 33 (95% confidence limits: 24-46) mumol.L-1. The time constant of IKs-tail deactivation was (92 +/- 18) ms in the control and (84 +/- 16) ms in the presence of Dau 30 mumol.L-1 (n = 8 cells from 4 animals, P > 0.05). (3) Addition of Dau 30 mumol.L-1 induced block of IKs and IKs-tail (n = 7 cells from 3 animals). The degree of block of IKs and IKs-tail depended on test potentials, increasing with more positive depolarizations. (4) Dau 20 mumol.L-1 blocked mainly inward component of IKl and reduced the reversal potential from -72 mV (control) to -78 mV (n = 6 cells from 3 animals). CONCLUSION: (1) Dau inhibited IKs, but not the process of IKs deactivation. (2) Dau blocked IKr, but not the process of deactivation. (3) Dau had a blocking effect on IKl.     

葛根素抗谷氨酸对小鼠神经细胞兴奋毒的作用

AIM: To study the effects of puerarin (Pue) against injury of cultured neurons by sodium glutamate (Glu). METHODS: Neuronal damage induced by Glu, N-methyl-D-asparate (NMDA), and kainic acid (KA), as well as the actions of Pue and some excitatory amino acid antagonists (EAAA), were measured by determining the leakage of lactate dehydrogenase (LDH) from nerve cells. RESULTS: The 24-h leakage of LDH was increased from cells exposed either to Glu 100 and 500 mumol.L-1 for 15 min (from 20 +/- 4 kU/g protein in control group to 35 +/- 3 kU/g protein in Glu 100 mumol.L-1 group and to 46 +/- 6 kU/g protein in Glu 500 mumol.L-1 group) or to NMDA 500 mumol.L-1 or KA 500 mumol.L-1 for 45 min (from 19 +/- 4 kU/g protein in control group to 27 +/- 3 kU/g protein in NMDA group and to 30 +/- 5 kU/g protein in KA group). Pre and post-treatment with Pue (100 mumol.L-1) decreased the leakage of LDH, which was similar to the effects of EAAA kynurenic acid (from 35 +/- 3 kU/g protein in Glu 100 mumol.L-1 to 20 +/- 5 kU/g protein in kynurenic acid group and to 22 +/- 3 kU/g protein in Pue group), DL-2-amino-5-phosphonovaleric acid (APV) (from 27 +/- 3 kU/g protein in NMDA damaged group to 183 kU/g protein in APV group and to 19 +/- 5 kU/g protein in Pue group) or 6,7-dinitroquinoxaline-2,3(1H,4H)-diane (DNQX) (from 30 +/- 5 kU/g protein in KA damaged control to 22 +/- 5 kU/g protein in DNQX group and to 20 +/- 4 kU/g protein in Pue group). Post-treatment with Pue (100 mumol.L-1) was able to reduce 24-h leakage of LDH from neurons expos ed to Glu 100 mumol.L-1 for 15 min (from 35 +/- 3 kU/g protein to 27 +/- 4 kU/g protein). CONCLUSION: Pue had protective effects on neurons damaged by Glu, NMDA, or KA.     

血小板活化因子诱导血小板P—选择素表达及相关信号传导机制

AIM: To study the intracellular signal transduction mechanisms of platelet activating factor (PAF)-induced platelet P-selectin expression. METHODS: Human blood platelets were used to test the effect of PAF-induced P-selectin expression using flow cytometry. RESULTS: PAF 20 nmol.L-1 elicited a moderate upregulation of P-selectin expression [(47.5 +/- 1.3)% vs control (3.8 +/- 0.9)%, P < 0.01]. Pretreatment with egtazic acid (EGTA) 2 mmol.L-1 and 5,5'- dimethyl-bis-(o-aminophenoxy)-ethane-N,N,N',N'-tetracetic acid (BAPTA) 200 mumol.L-1 to block Ca2+ influx or chelate the intracellular calcium, respectively, reduced P-selectin expression in response to PAF [(13.3 +/- 0.9)% and (16.8 +/- 1.9)% vs (47.5 +/- 1.3)% of PAF group, P < 0.01]. Inhibition of Na+/H+ exchange with amiloride (Ami) 400 mumol.L-1 resulted in an inhibition of P-selectin expression [(37.5 +/- 2.1)% vs (47.5 +/- 1.3)% of PAF group, P < 0.01]. Genistein (Gen) 300 mumol.L-1 to inhibit protein tyrosine phosphorylation showed similar effect [(29 +/- 4)% vs (47.5 +/- 1.3)% of PAF group, P < 0.01]. CONCLUSION: Multiple signal transduction pathways, including protein tyrosine phosphorylation, Na+/H+ exchange, and Ca2+ mobilization, mediated PAF-induced P-selectin expression.     

苄基四氢巴马汀对豚鼠心室肌细胞快激活延迟整流钾电流的作用

目的研究苄基四氢巴马汀(BTHP)对心室肌细胞快激活(I_kr)延迟整流钾电流的作用。方法 用全细胞膜片钳技术记录豚鼠心室肌细胞钾离子通道电流。结果BTHP在1～100 μmol·L^-1以浓度依赖性方式阻滞I_kr,其IC₅₀为13.5 μmol·L^-1(95%可信范围:11.2～15.8 μmol·L^-1)。30 μmol·L^-1 BTHP可使I_kr及I_kr,tail分别降低(31±4)%和(36±5)% (N=6,P<0.01)。与多数III类抗心律失常药物不同,BTHP可频率依赖性地抑制I_kr。该药主要改变I_kr的失活过程,可使I_kr的失活时间常数(τ)从(238±16) ms降至(196±14) ms,而对I_kr的激活动力学影响不大。结论BTHP对I_kr有明显的抑制作用,且其阻滞作用呈现频率依赖性特征。