牛磺酸对缺血大鼠心肌线粒体Ca^2＋—Mg^2＋—ATP酶活性与MDA …

目的和方法：用Ｗｉｓｔａｒ大鼠皮下注射异丙肾上腺素（ＩＳＰ,５ｍｇ／ｋｇ）诱导心肌缺血模型。观测心肌线粒体（Ｍｉｔ）中丙二醛（ＭＤＡ）含量、Ｃａ＾２＋－Ｍｇ＾２＋－ＡＴＰ酶和Ｃａ＾２＋－Ｍｇ＾２＋－ＡＴＰ酶和Ｃａ＾２＋－ＡＴＰ酶活性及牛磺酸（Ｔａｕ）的影响。结果：缺血组大鼠心肌Ｍｉｔ中ＭＤＡ升高８７．８３％、Ｃａ＾２＋－Ｍｇ＾２＋－ＡＴＰ酶和Ｃａ＾２＋－ＡＴＰ酶活性分别降低３７．５６％和５０．２０     

牛磺酸对缺血大鼠心肌线粒体Ca2+-Mg2+-ATP酶活性与MDA含量影响

目的和方法：用Ｗｉｓｔａｒ大鼠皮下注射异丙肾上腺素（ＩＳＰ,５ｍｇ／ｋｇ）诱导心肌缺血模型。观测心肌线粒体（Ｍｉｔ）中丙二醛（ＭＤＡ）含量、Ｃａ２＋－Ｍｇ２＋－ＡＴＰ酶和Ｃａ２＋－ＡＴＰ酶活性及牛磺酸（Ｔａｕ）的影响。结果：缺血组大鼠心肌Ｍｉｔ中ＭＤＡ升高８７８３％、Ｃａ２＋－Ｍｇ２＋－ＡＴＰ酶和Ｃａ２＋－ＡＴＰ酶活性分别降低３７５６％和５０２０％（Ｐ＜０．０１）。Ｃａ２＋－Ｍｇ２＋－ＡＴＰ酶活性与ＭＤＡ含量也呈显著负相关（ｒ＝－０．８７,Ｐ＜０．０１）。Ｃａ２＋－ＡＴＰ酶活性与ＭＤＡ含量也呈显著负相关（ｒ＝－０７９,Ｐ＜０．０１）。在注射异丙肾上腺素（ＩＳＰ）前３０ｍｉｎ腹腔注射Ｔａｕ（２００ｍｇ／ｋｇ）则Ｍｉｔ中ＭＤＡ含量、Ｃａ２＋－Ｍｇ２＋－ＡＴＰ酶和Ｃａ２＋－ＡＴＰ酶活性均未见显著异常改变。结论：Ｔａｕ可能通过抑制ＭＤＡ的生成实现其保护Ｃａ２＋－ＡＴＰ酶和Ｃａ２＋－Ｍｇ２＋－ＡＴＰ酶活性的作用。     

粗氨酸加压素对慢性肾衰大鼠心功能及其心肌细胞钠—钾—ATP酶…

用ＳＤ大鼠制作慢性肾衰（ＣＲＦ）动物模型，观察其乐与心肌精氨酸加压素（ＡＶＰ）含量的变化；ＣＲＦ大鼠静脉分别注射ＡＶＰ及其抗血清，观察其对平均动脉压、左心室压峰值和心肌细胞钠－钾－ＡＴＰ酶（Ｎａ＾＋，Ｋ＾＋－ＡＴＰ酶）活力的影响。结果表明，ＣＲＦ大鼠血浆及心肌ＡＶＰ含量与血肌酐水平同步增高；静脉注射ＡＶＰ标准品，可使心ａ＾＋，Ｋ＾＋－ＡＴＰ酶活力明显降低，并加重心功能指标的异常变化，而给予ＡＶＰ抗     

尼群地平对体外循环中红细胞钙及变形能力的影响

研究体外循环中钙桔抗剂对红细胞的影响。方法：对４０例非紫绀型先天性心脏病患者,按随机配对原则分为对照组（Ｃ组）与尼群地平组（Ｎ组）。测定体外循环期红细胞钙（Ｅ－Ｃａ２＋）、Ｃａ２＋,Ｍｇ２＋－ＡＴＰ酶与Ｎａ＋,Ｋ＋－ＡＴＰ酶活性、滤过指数（ＩＦ）、平均体积（ＭＣＶ）。结果：Ｃ组体外循环中Ｅ－Ｃａ２＋、ＩＦ、ＭＣＶ进行性增加,Ｃａ２＋,Ｍｇ２＋－ＡＴＰ酶与Ｎａ＋,Ｋ＋－ＡＴＰ酶活性下降,Ｅ－Ｃａ２＋与ＩＦ、ＭＣＶ直线正相关,而Ｎ组上述各项指标变化均明显减轻（Ｐ＜０．０５）。结论：结果提示体外循环中尼群地平对红细胞具有良好的保护作用。     

地奥心血康对心肌缺血再灌犬心肌细胞膜Na^＋,K^＋—ATP酶活…

１６只成年杂种犬复制心肌缺血再灌模型。分为地奥心血康治疗组（ＤＡＸＸＫＧ）和生理盐水对照组（ＮＳＣＧ）。差速离心分离肌细胞质膜，无机磷法测定心肌细胞膜Ｎａ＾＋、Ｋ＾＋－ＡＴＰ酶活性，荧光法测定心肌细胞膜在清脂质过氧化物（ＬＰＯ）含量。结果表明：（１）ＤＡＸＸＫＧ Ｎａ＾＋，Ｋ＾＋－ＡＴＰ酶活性明显高于ＮＳＣＧ（Ｐ〈０．０１）；（２）血清ＬＰＯ含量，随着再灌时间延长，ＮＳＣＧ呈上升趋势，ＤＡＸＸＫＧ     

预缺氧对急性缺氧大鼠心肌线粒体功能及ATP含量的影响

目的：观察预缺氧对急性缺氧大鼠心肌线粒体功能及ＡＴＰ含量的影响。方法：实验大鼠分三组。１常氧对照组;２急性缺氧组;３预缺氧组。测定了心肌ＡＴＰ含量及线粒体呼吸功能,以荧光偏振法测定线粒体膜流动性。结果：经预缺氧处理的大鼠遭受急性缺氧后ＡＴＰ含量从（３１８±２４２）ｍｇ１·ｇ－１增加到（６０５５±３．５２）ｍｇ－１·ｇ－１（Ｐ＜００１）;线粒体呼吸控制率（ＲＣＲ）从１８４±０５８上升到４５５±０３２（Ｐ＜００１）;线粒体膜流动性（ＭＭＦ）明显增加（Ｐ＜００５）,Ｆ０Ｆ１－ＡＴＰ酶及Ｎａ＋－Ｋ＋－ＡＴＰ酶活性分别提高６６％和２５％。结论：预缺氧可有效改善缺氧大鼠心肌能量代谢,其作用环节可能和提高线粒体膜流动性,改善线粒体呼吸功能有关。     

内毒素对兔骨骼肌细胞外液容积,钠钾离子及其Na^＋—K^＋—ATP酶活性…

本实验以氚水和Ｎａ２＾３５ＳＯ４为标记物，观察了内毒素对兔骨骼肌细胞外液容积（ＥＣＶ）、Ｎａ＾＋，Ｋ＾＋含量以及（Ｎａ＾＋－Ｋ＾＋）－ＡＴＰ酶活性的影响。实验结果显示，动物静注内毒素（０．５ｍｇ／ｋｇ）后１０小时骨骼肌ＥＣＶ、Ｎａ＾＋，Ｋ＾＋含量和（Ｎａ＾＋－Ｋ＾＋）－ＡＴＰ酶活性均无显著变化；但血Ｋ＾＋浓度自内毒素注射后３小时即有显著下降。     

dt2—cAMP,IFN—γ和PMA对U937胞浆Ca^2＋和酪氨酸激？…

目的 探讨ｄｔ２－ｃＡＭＰ，ＰＭＡ和ＩＦＮ－γ对Ｕ９３７细胞Ｃ５ａＲ表达的影响，以及ｒｈＣ５ａ刺激受ｄｔ２－ｃＡＭＰ，ＰＭＡ和ＩＦＮ－γ分化的Ｕ９３７细胞后，其胞浆Ｃａ＾２＋浓度的变化情况。方法 用流式细胞仪分析胞膜Ｃ５ａＲ和细浆蛋白酪氨酸激酶的表达；荧光发光法测定胞浆Ｃａ＾２＋浓度的变化。结果 ｄｔ２－ｃＡＭＰ，ＰＭＡ和ＩＦＮ－γ等可不同程度地上调Ｃ５ａＲ表达。用０．５ｍｍｏｌ／Ｌ的ｄｔ２－ｃＡ     

糖尿病大鼠心肌MDA含量,SOD和Na—K—ATP酶活性的变化

实验用四氧嘧啶破坏Ｗｉｓｔａｒ大鼠胰腺发诱导糖尿病模型，观察糖尿病大鼠心肌组织ＭＤＡ含量，ＳＯＤ和Ｎａ＾＋－Ｋ＾＋－ＡＴＰ酶活性的变化以及氧自由基清除剂（ＶｉｔＥ，亚硒酸钠）对糖尿病大鼠心肌的保护作用，结果表明：（１）糖尿病大鼠心肌组织ＭＤＡ含量显著增加（Ｐ〈０．０５），而心肌细胞膜上Ｎａ＾＋－Ｋ＾＋－ＡＴＰ酶的活性显著下降（Ｐ〈０．０１），（２）ＶｉｔＥ和亚硒酸钠能显著降低糖尿病大鼠心肌组织ＭＤ     

绞股蓝总皂甙抗大鼠海马结构缺血再灌注损伤的实验研究

探讨大鼠海马结构缺轿再灌注损伤机理及绞股蓝总皂甙抗缺血再灌注损伤的作用，结果：ＩＲ组海马组织中ＭＤＡ含量高于组（Ｐ〈０．０１），而ＳＯＤ含量低于ＳＯＣ组（Ｐ〈０．０１），差异非常显著：ＩＲ＋ＧＰ组海马组织中ＭＤＡ含量明显低于ＩＲ组（Ｐ〈０．０１），而ＳＯＣ含量明显高于ＩＲ组（Ｐ〈０．０１），ＩＲ组海马组织Ｎａ＾＋－Ｋ＾＋－ＡＴＰａｓｅ，Ｃａ＾２＋－ＡＴＰａｓｅ的活性明显低于ＳＯＣ组（Ｐ〈０．０１）     

妊高征患者血浆ET水平与红细胞膜ATP酶活性的改变与发生肾病的关系

目的：探讨了妊高征肾病患者血浆内皮素（ET）水平和红细胞膜ATP酶活性的改变参与妊高征肾病的可能机制。方法：应用放射免疫分析和Reilni制膜法制定了32例妊高征肾病患者血浆ET水平和红细胞膜上Na^＋-K^＋-ATP酶和Ca^2＋-Mg^2＋-ATP酶活性的变化，并与70名妊高征无肾病组和35名正常孕妇作比较。结果：妊高征肾病组和无肾病组血浆ET水平非常显著地高于正常孕妇组（P〈0．01），而红细胞膜上Na^＋K^＋-ATP酶和Ca^2＋-Mg^2＋-ATP酶的活性均显著地低于正常孕妇组（P〈0．01），妊征肾病组与无肾病组有显著性差异（P〈0．05）。结论：妊高征肾病的发生与发展与血浆ET和红细胞膜上Na^＋-K^＋-ATP酶和Ca^2＋-Mg^2＋-ATP酶的活性有密切的关系。     

血小板活化因子在急性胰腺炎大鼠肺损伤发病中作用

以牛磺胆酸钠诱发大鼠急性胰腺炎并发肺损伤模型，观察血小板活化因子拮抗剂ＢＮ５２０２１对肺病理形态、肺系数、血小板聚集率及肺血流量的影响，记录其大鼠存活率。结果表明，ＢＮ５２０２１治疗后，胰腺出血坏死程度减轻同时肺损伤显著改善，肺系数值、血小板聚集率显著低于急性胰腺炎非治疗组，肺相对血流量及组织灌注量显著高于急性胰腺炎非治疗组，大鼠存活率提高。提示内源性血小板活化因子通过增加肺血管通透性、影响肺血循环而介导急性胰腺炎大鼠肺损伤。     

The effect of the platelet-activating factor antagonist, BN 52021, on human natural killer cell-mediated cytotoxicity.

The influence of the platelet-activating factor (PAF) antagonist, BN 52021, on human natural killer (NK) cell cytotoxicity against K 562 target cells was determined. Cytotoxicity was measured by a short-term (4 hr) 51Cr-release assay. The cytotoxicity was significantly reduced in the presence of PAF antagonist at concentrations from 30 to 120 microM. This reduction of killing was not due to the impairment of binding of effector cells to target cells. Pretreatment of K 562 target cells with the PAF antagonist led to a greater inhibition of NK cell cytotoxicity compared with that observed when the effector cells were preincubated with BN 52021. Thus, the inhibition of cytotoxicity appears to be due to an effect of BN 52021 on target cells rather than on lymphocytes. Furthermore, the increase in NK activity induced by interferon was less pronounced when BN 52021 was added in the incubation medium. The natural cytotoxicity of platelet-depleted or large granular lymphocyte-enriched effector cell populations was inhibited by the PAF antagonist in a similar manner. The effect of BN 52021 appears to be related to its specific PAF antagonistic activity since a similar action on NK cells was noted with two other structurally unrelated PAF antagonists, BN 52111 and WEB 2086. In contrast, Ginkgolide J (BN 52024), which is structurally related to BN 52021 but lacks PAF antagonistic activity, was ineffective in inhibiting NK cell cytotoxicity. Finally, synthetic PAF induces a dose-dependent cytotoxic action on K 562 cells and this effect of the autacoid is inhibited by BN 52021. These observations provide indirect evidence that PAF could play a role in the mechanism(s) of NK cytotoxity.     

还少丹对D-半乳糖致衰小鼠心肌线粒体结构与功能的影响

目的:探讨还少丹对D-半乳糖(D-galactose,D-gal)诱导的衰老模型小鼠心肌线粒体结构与功能的影响.方法:将小鼠随机分为空白对照组、衰老模型组、还少丹低、高剂量组.采用D-gal建立衰老模型,还少丹水煎液灌胃6周.以差速离心法分离小鼠心肌组织线粒体;Comas亮蓝蛋白定量法测定线粒体蛋白含量;分光光度法检测...     

肾阳虚证患者红细胞LPO、SOD和ATP酶活性的变化

目的 :探讨肾阳虚证患者红细胞LPO、SOD和ATP酶活性的特点及其意义。方法 :观察 19例肾阳虚证患者和 2 1例正常人红细胞LPO、SOD和红细胞膜Na+ K+ ATP酶、Mg2 + ATP酶、Ca2 + ATP酶、Ca2 + Mg2 + ATP酶活性的变化。结果 :与对照组比较 ,肾阳虚证患者红细胞LPO含量升高 (P <0 .0 1) ,红细胞SOD活性降低 (P <0 .0 1) ;红细胞膜Na+ K+ ATP酶活性显著升高 (P <0 .0 1) ,而Mg2 + ATP酶活性变化无显著性差异 ,Ca2 + ATP酶活性升高 (P <0 .0 1) ,Ca2 + Mg2 + ATP酶活性也显著升高 (P <0 .0 1)。结论 :肾阳虚证患者红细胞内脂质过氧化反应增强 ,而抗氧化能力降低 ,红细胞膜Na+ K+ ATP酶、Ca2 + ATP酶和Ca2 + Mg2 + ATP酶活性升高 ;本研究为理解肾阳虚证的病理生理基础提供了初步实验依据     

Protection of platelet-activating factor-induced acute renal failure by BN 52021.

Although platelet-activating factor (PAF) is a well-known mediator in experimental shock, its precise role in acute renal failure remains to be defined. Male Wistar rats (209 +/- 12 g) were placed in individual metabolic cages for 24 h before i.v. injection of PAF (2-6 micrograms/kg). Injection of 6 micrograms/kg PAF proved lethal and use of such a high dose was thus discontinued. Administration of 2 micrograms/kg and 4 micrograms/kg PAF resulted in a fall of glomerular filtration rate (GFR) associated with a reduction in urinary flow rate (UFR). Rats pretreated with BN 52021 (25 mg/kg p.o.) exhibited values of GFR similar to that of the control group, but not after 4 micrograms/kg PAF. In addition, in the group of BN 52021 pretreated rats and injected with 2 micrograms/kg or 4 micrograms/kg PAF, UFR was not significantly different from that of the control group at 24 h. Examination by electron microscopy revealed the presence of platelets in the glomeruli, as well as loss of fixed anionic charges in PAF injected rats. The presence of these platelets was not observed in rats treated with BN 52021 and injected with PAF. No changes in GFR and UFR were observed at 6 h or 24 h in vehicle or BN 52021 treated rats. Thus, BN 52021 which affords protection against acute renal failure induced by PAF may be of therapeutic value in other types of kidney disease in which this mediator is active.     

新城疫病毒对BGC-823胃癌细胞线粒体的影响

目的 探讨新城疫病毒对BGC-823胃癌细胞线粒体结构和三磷酸腺苷(ATP)酶活性等功能的影响.方法 应用电子显微镜观察、线粒体Na+-K+-ATP酶、Ca2+-ATP酶活性变化测定、罗丹明123染色法测定细胞线粒体膜电位及Western Blot测定细胞色素C等方法 进行分析.结果 新城疫病毒感染肿瘤细胞线粒体结构破坏,线粒体Na+-K+ATP酶、Ca2+-ATP酶活性较对照组显著下降(P<0.01).线粒体膜电位及细胞色素C显著下降(P<0.01).结论 对线粒体结构及功能的影响可能是新城疫病毒杀伤BGC-823胃癌细胞的机制之一.     

Involvement of platelet-activating factor and tumour necrosis factor in the pathogenesis of joint inflammation in rabbits.

We have studied the participation of platelet-activating factor (PAF) in antigen-induced arthritis in rabbits, as well as the possible co-operation between PAF and tumour necrosis factor (TNF) in their ability to induce joint inflammation when injected into the knees of healthy rabbits. The administration of two structurally different PAF receptor antagonists, BN52021 and Alprazolam, from 4 h before the intra-articular injection of ovalbumin in preimmunized rabbits, induced an important reduction in the synovial fluid volume, in the amount of cells infiltrating the articular cavity and the synovial membrane, as well as in the prostaglandin E2 (PGE2) concentration. Furthermore, proteoglycans of the articular cartilage, which were found diminished in animals with non-treated arthritis, were well preserved in rabbits treated with PAF antagonists. All the synovial fluids from joints with arthritis had detectable amounts of PAF. The injection of either TNF or PAF into the joints of normal rabbits induced a mild inflammation. When TNF was administered 1 h before PAF, a synergistic response was noted in the synovial fluid volume, in the accumulation of leucocytes, and in the amount of PGE2. The administration of BN50726, a hetrazepine with a potent PAF-receptor antagonist effect, induced a diminution in those parameters. Our results suggest that PAF may be an early and important mediator of joint damage, and that TNF can amplify the inflammatory response induced by PAF. PAF receptor antagonists could play some role in the treatment of inflammatory joint diseases.     

BN52021 protects rat cardiomyocyte from doxorubicin induced cardiotoxicity

The aim of this study was to assess the role of platelet activating factor (PAF) antagonist BN52021 in doxorubicin induced cardiotoxicity and to explore the mechanisms. H9c2 cardiomyocytes were employed to investigate the effect of BN52021 on doxorubicin induced cell viability and cell apoptosis. Signaling pathway of caspase 3, cytochrome c, calcium and p38 mitogen-activated protein (MAPK) was determined during the doxorubicin induced apoptosis. Our results showed BN52021 pretreatment could protected cell death induced by doxorubicin in H9c2 cardiomyocytes. Decrease concentration of [Ca²⁺] and expression of phosphorylated P38 MAPK were accounted for the protection effect. Inhibition of signaling pathway of calcium and p38 MAPK showed similar effect exerted by BN52021 in doxorubicin induced cell apoptosis. Our results demonstrated BN52021 protected against doxorubicin induced cell death in H9c2 cardiomyocytes by calcium and p38 MAPK signaling in vitro. These finding may give insight on the treatment of doxorubicin induced cardiomyopathy.     

Characterization of Mg-ATP-dependent Ca2+ transport in cat pancreatic microsomes

Mg-ATP-dependent 45Ca2+ uptake and Ca2+-ATPase activity have been examined in isolated microsomes obtained by differential centrifugation and in purified subcellular fractions obtained by Ficoll-sucrose density centrifugation in the presence of mitochondrial inhibitors. Mg-ATP-dependent 45Ca2+ uptake increased with increasing EGTA-buffered free [Ca2+], reaching a maximum of 2 nmol 45Ca2+ X 15 min-1 X mg prot-1 at 2 mumol/1 [Ca2+] in the incubation medium. Half-maximal 45Ca2+ uptake was at approximately 0.2 mumol/1 [Ca2+]. Maximal Ca2+ -Mg2+ -ATPase activity was 130 nmol X 15 min-1 X mg prot-1 at 2 mumol/l [Ca2+], with an apparent Km of approximately 0.3 mumol/l [Ca2+]. The Ca2+ ionophore A23187 (10(-6) mol/l), the mercurial compounds mersalyl (10(-5) mol/l) and CH3ClHg (10(-3) mol/l), as well as La3+ (10(-4) mol/l), vanadate (10(-4) mol/l), and saponin (50 micrograms/mg prot), abolished Mg-ATP-promoted 45Ca2+ uptake. In the absence of Mg2+, ATP did not provoke 45Ca2+ uptake. Using the purified smooth membrane fraction (F1) from the Ficoll-sucrose density gradient (enrichment of Na+-K+-ATPase specific activity by ninefold and of NADH-cytochrome c reductase by threefold as compared with total tissue homogenate), Mg-ATP-dependent 45Ca2+ uptake correlated better with Na+-K+-ATPase (r = 0.97) than with the smooth endoplasmic marker NADH-cytochrome c reductase (r = 0.52). No correlation was found with RNA, the marker for rough endoplasmic reticulum. We conclude that pancreatic plasma membranes contain a Ca2+-Mg2+-ATPase that represents the Ca2+ extrusion system from acinar cells. It is also possible that vesicular membrane structures associated with the plasma membrane, or endocytotic plasma membrane vesicles, take up Ca2+ and represent an intracellular Ca2+ pool.