人参茎叶皂甙在体外对兔脑Ca~(2+)-ATP酶和Mg~(2+)-ATP酶活力的影响

体外实验发现,人参茎叶总皂甙(GNS)、人参茎叶三醇组皂甙(PTS)均能显著抑制兔大脑Ca~(2+)-ATP酶和Mg~(2+)-ATP酶的活力;而人参茎叶二醇组皂式(PDS)在10和100mg/L时,显著兴奋Ca~(2+)—ATP酶的活力,在1000mg/L时,则显著抑制Ca~(2+)—ATP酶活力,对Mg~(2+)-ATP酶的活力也具有抑制作用;氯丙嗪(CPZ,0.35和0.70mmol/L)对Ca~(2+)-ATP酶和Mg~(2+)—ATP酶的活力均呈现非常显著的抑制作用。     

人参与三七总皂甙对大鼠肾脏微粒体Na~+,K~+-ATP酶的抑制作用

<正> 人参(Panax schinseng Nees)具有抗利尿作用,可导致水钠潴留、排钾及钠/钾比值降低,该作用由人参总皂甙产生,但其分子作用机理仍不清楚。已知一些药物系通过对肾脏Na~+,K~+-ATP酶的抑制,导致水钠潴留,尿钾增加。本文研究人参总皂甙对大鼠肾脏微粒体Na~+,K~+-ATP酶活力的影响,以探讨人参影响肾脏电解质平衡的作用机理,并和从三七(Panax pseudo-ginseng Wall.     

类固醇性激素对豚鼠心室肌细胞膜Na~+,K~+—ATPase活力影响

采用 Harry 法测定无机磷含量,间接测定心肌细胞膜 Na~+,K~+—ATPase 酶活力,结果表明,性激素对心肌细胞膜 Na~+,K~+—ATPase 活力均有抑制作用。说明性激素可以使心肌细胞膜上的 Na~+,K~+—ATPAase 活力下降。     

低浓度毒毛旋花子苷元的强心作用及其与心肌细胞膜Na~＋，K~＋-ATP酶的关系

目的:观察低浓度的毒毛旋花子苷原(Strophanthidin,Str)对离体豚鼠心脏是否有强心作用,及其与心肌细胞膜Na~+,K~+-ATP酶活性的关系。方法:采用Langendorff离体灌流装置经主动脉逆行灌流心脏;八道生理记录仪记录心率(HR),左室内压(LVP)及其最大变化速率(±dP/dt_(max));无机磷法测定心肌细胞膜Na~+,K~+-ATP酶活性。结果:Str 0.1nmol/L可兴奋Na~+,K~+-ATP酶活性(P<0.05)但不影响心脏的收缩功能,Str 1nmol/L仅能升高+dP/dt_(max)(P<0.05)并兴奋Na~+,K~+-ATP酶活性(P<0.01),Str 10和100 nmol/L可升高LVP和+dP/dt_(max)(P<0.05或P<0.01),对Na~+,K~+-ATP酶活性无明显作用,Str 1-100μmol/L虽能短暂升高LVP和±dp/dt_(max)(P<0.01),但随后出现不规则收缩并使LVP和±dP/dt_(max)降低,其对Na~+,K~+-ATP酶活性则表现为剂量依赖性抑制作用(P<0.01)。结论:高浓度Str的正性肌力作用是通过抑制Na~+,K~+-ATP酶活性实现的,而低浓度Str的强心作用似与Na~+,K~+-ATP酶抑制作用无关。     

性激素对豚鼠心肌细胞膜Na~+,K~+-ATP酶活力的影响

采用Matsui and Schwartz方法制备Na~+,K~+—ATP酶液,Harry法测定无机磷含量,间接测定心肌细胞膜Na~+,K~+—ATP酶活力,实验结果表明,丙酸睾丸素、已烯雌酚对心肌细胞膜Na~+,K~+—ATP酶活性均有明显的抑制作用。但丙酸睾丸素呈正相关,已烯雌酚呈负相关,说明性腺激素可以使心肌细胞膜上的Na~+,K~+—ATP酶活性降低。     

几种人参皂甙对大鼠肾脏微粒体Na~+,K~+-ATP酶的抑制作用

人参皂甙Rg组、Rb组、Rg_1、Rb_1对大鼠肾脏微粒体Na~+,K~+—ATP酶均有抑制作用,IC_(50)分别为402,74μg/ml,15和50μmol/L。Rb组、Rg_1和Rb_1的抑酶作用可逆;增加K~+可竞争性拮抗Rg_1和Rb_1的抑酶作用,但Na~+对此作用无明显影响。动力学研究表明,Rg_1和Rb_1抑制Na~+,K~+—ATP酶,对底物ATP似为反竞争性抑制剂。     

特异性单克隆抗体对地高辛抑制家兔红细胞膜Na~+,K~+-ATP酶活性的拮抗作用

本文研究结果表明抗地高辛特异性MAb可有效地拮抗地高辛引起的RRBC膜Na~+,K~+-ATP酶活性抑制。1.8×10~4倍稀释的FD8 MAb腹水,在试管内可使4ng/ml浓度地高辛引起的酶活性抑制恢复达50％。给地高辛中毒兔iv FD8 MAb 腹水后,被抑制的RRBC膜Na~+,K~+-ATP酶活性迅速恢复,酶抑制造成的RRBC内Na~+,K~+浓度异常也随之得到恢复。本研究从受体水平证实了特异性MAb解除地高辛毒性的作用机理     

蜂毒肽对豚鼠心肌线粒体Na~ 、K~ -ATP酶的影响(英文)

目的:研究蜂毒肽对豚鼠心肌线粒体Na~ ,K~ -ATP酶活性的影响。方法:应用光电比色法测定Na~ ,K~ -ATP酶活性。以Line-weaver-burk双倒数作图法分析酶动力学参数。结果:蜂毒肽抑制心肌Na~ ,K~ -ATP酶表现为浓度和时间依赖性,IC_(50)为2.60μmol/L。酶动力学研究表明,蜂毒肽对Na~ ,K~ -ATP酶有抑制作用,对K~ 表现为竞争性结合,对Na~ 及ATP表现为非竞争性结合。结论:蜂毒肽对心肌Na~ ,K~ -ATP酶有抑制作用,其抑制机制主要是与K~ 竞争结合酶外侧的K~ 结合位点。     

丹酚酸A对胃H~+,K~+-ATP酶的作用

从丹参Salvia militiorrhiza的水提物中分离出一个缩酚酸类成分-丹酚酸A,药理研究表明它具有抑制H~+,K~+-ATP酶的作用。本文就其对胃的H~+,K~+-ATP酶、胃酸分泌和实验性溃疡模型的作用进行了深入研究。 (1)对H~+,K~+-ATP酶的作用:丹酚酸A对于由猪胃粘膜中获得的H~+,K~+-ATP酶的抑制呈剂量依赖性,IC_(50)为5.2×10~(-7)mol。丹酚酸A上的六个羟基的乙酰化可使其活性完全消失。 (2)抑制H~+,K~+-ATP酶的动力学研究:为弄清丹酚酸A作用类型,考察了ATP和     

白藜芦醇对大鼠脊髓急性损伤后继发性损伤的影响

目的:探讨脊髓损伤(SCI)后使用白藜芦醇(resveratrol, Res)对继发性脊髓水肿、受损脊髓组织中乳酸脱氢酶(LDH)与Na~+,K~+-ATP酶活性及早期脂质过氧化反应的影响。方法:采用重物下落撞击法制备成年大鼠的脊髓损伤模型,于损伤后即刻腹腔注射Res(50mg/kg,100mg/kg)或甲基强的松龙(MPSS,100mg/kg),观察给药后1h、24h、48h时Res组受损脊髓组织含水量、LDH与Na~+,K~+-ATP酶活性及MDA水平的变化,同时用电子显微镜观察超微结构的变化,并与MPSS组进行疗效对比。结果:Res显著抑制SCI后继发性水肿,48h最明显(P<0.05),抑制率为11.5％;显著降低LDH活性,24h时最大(P<0.01),抑制率大于40％;明显改善Na~+,K~+-ATP酶活性,以48h最显著(P<0.01),最大改善率在60％以上;显著抑制SCI后MDA产生,48小时为最明显(P<0.01),Res在50mg/kg和100mg/kg的剂量情况下所表现的上述作用比100mg/kg的MPSS更佳,电子显微镜的结果表明,Res和MPSS能有效保护SCI后脊髓组织的超微形态结构的正常性。结论:Res有效抑制脊髓损伤后的水肿和早期受损局部脂质过氧化反应并改善能量代谢系统,因此对脊髓损伤有潜在的治疗作用。     

Prednisolone-3, 20-bisguanylhydrazone: Na+, K+-ATPase inhibition and positive inotropic action.

The relationship between two known actions of prednisolone-3, 20-bisguanylhydrazone (PBGH); Na+, K+-ATPase inhibition and positive inotropic effects, was investigated. In electrically driven left atrial preparations of guinea pig heart, the positive inotropic action of PBGH was not affected by beta-adrenergic or histamine antagonists. Pretreatment of animals with reserpine also failed to influence the positive inotropic action of PBGH. Inotropic concentrations of PBGH inhibited Na+, K+-ATPase and the ATP-dependent binding of (3/)-ouabain to Na+, K+- ATPase preparations in vitro. Additionally, ouabain-sensitive 86Rb uptake, an estimate of sodium pump activity was inhibited when sodium-loaded ventricular slices were obtained from Langendorff preparations at the peak inotropic response to PBGH. Guinea pig heart was highly sensitive to PBGH to the positive inotropic action, the inhibition of Na+, K+ -ATPase and (3H)-ouabain binding, whereas rat, rabbit and dog heart were markedly less sensitive. These findings suggest that the mechanism of the positive inotropic action of PBGH resembles that of ouabain and probably involves Na+, K+ -ATPase inhibition, although the mode of interaction of these steroids with Na+, K+ -ATPase may be different.     

Inhibitory effects of ginsenoside Rg1 and Rb1 on rat brain microsomal Na+,K(+)-ATPase activity

Rat brain microsomal Na+, K(+)-ATPase activity was inhibited significantly and rapidly by ginsenoside Rb1. The IC50 of Rb1 for Na+,K(+)-ATPase was 6.3 +/- 1.0 mumol/L. The inhibition was enhanced with increasing the concentration of Rb1 or decreasing that of Na+ and K+. Kinetic analysis revealed that ginsenoside was an uncompetitive inhibitor with respect to ATP. The inhibitory effect of Rg1 on rat brain microsomal Na+,K(+)-ATPase was much weaker than that of Rb1.     

l-Cysteine and glutathione restore the modulation of rat frontal cortex Na, K-ATPase activity induced by aspartame metabolites

BACKGROUND: Studies have suggested that aspartame (ASP) ingestion is implicated in neurological problems. AIM: The aim of this study was to evaluate rat frontal cortex Na+, K+ -ATPase and Mg2+ -ATPase activities after incubation with ASP or each of its metabolites, phenylalanine (Phe), methanol (MeOH) and aspartic acid (asp) separately. METHOD: Suckling rat frontal cortex homogenates or pure Na+, K+ -ATPase were incubated with ASP metabolites. Na+, K+ -ATPase and Mg2+ -ATPase activities were measured spectrophotometrically. RESULTS: Incubation of frontal cortex homogenate or pure Na+, K+ -ATPase with various ASP concentrations as expected in the cerebrospinal fluid (CSF) after ASP consumption of 34, 150 or 200mg/kg, decreased the frontal cortex enzyme activity by 33%, 53% or 57%, respectively, whereas pure enzyme was remarkably stimulated. Moreover, incubation of frontal cortex homogenate with each one of the expected ASP metabolites in the CSF, except MeOH, which are related to the intake of the above mentioned doses of the sweetener, resulted in an activation of the membrane Na+, K+ -ATPase, as well as pure enzyme. Frontal cortex Mg2+-ATPase remained unaltered. Addition of l-cysteine (cys) or reduced glutathione (GSH) to ASP metabolites mixtures, corresponding to 150 or 200mg/kg doses of the sweetener, completely or partially restored to normal the modulated membrane and pure Na+, K+ -ATPase activities. CONCLUSION: CSF concentrations of the sum of ASP metabolites corresponding to the intake of common, abuse or toxic doses (34 or 150 or 200mg/kg, respectively) of the additive significantly increased rat frontal cortex Na+, K+ -ATPase and pure enzyme activities. Cys or GSH completely or partially restored to normal both enzyme activities, possibly due to amelioration of the cellular GSH reduction from the action of MeOH, a metabolite of the sweetener and/or by their scavenging effect.     

In vivo and in vitro effects of cadmium on adult rat brain total antioxidant status, acetylcholinesterase, (Na+, K+)-ATPase and Mg2+-ATPase activities: protection by L-cysteine

This study was undertaken in order to investigate a) the short- and long-term in vivo effects of cadmium (Cd) on brain acetylcholinesterase (AChE), (Na+, K+)-ATPase activities in adult rats, b) the concentration-dependent in vitro and in vivo (acute experiment) effects of Cd on the activity of those enzymes, c) the in vivo and in vitro effects of the antioxidant L-cysteine (Cys) on the above enzyme activities, and d) the evaluation of brain total antioxidant status after in vivo Cd, L-cysteine, or L-cysteine+Cd administration in rats. In vitro, CdSO4 inhibited pure and brain AChE in concentrations higher than 0.1 mM, while it activated by approximately 70% (P<0.001) brain Na+, K+ -ATPase in concentrations up to 0.1 mM and inhibited its activity in higher concentrations. Mg2+ -ATPase was not influenced up to 0.1 mM concentration, while it was inactivated (40%, P<0.001) in higher CdSO4 concentrations. A dose-response study of brain CdSO4 (1,2 and 5 mg/kg once 8 hr before decapitation) revealed a dose-dependent decrease (-14 to -30%, P<0.001) of brain AChE activity, an increase of Na+, K+ -ATPase activity (+47 to +200%, P<0.001) and an increase of Mg2+ -ATPase only after the highest dose (5mg/kg) in the short-term treatment of rats. Long-term Cd administration (1 mg/kg rat daily for 4 months) activated brain AChE and Na+, K+ -ATPase about 50-65% (P<0.001) but not Mg2+ -ATPase. Brain total antioxidant status was decreased by Cd (30%, P<0.01), while it was increased by L-cysteine or L-cysteine+Cd (50%, P<0.001) in the short-term in vivo treatment. L-cysteine reversed the enzymatic activity changes observed with Cd alone in the high-dose short-term in vivo treatment of rats, as well as the brain AChE inhibition induced by Cd in the in vitro experiments. These results indicate that: a) Cd can influence in a different way the examined enzyme activities after short- and long-term administration, b) Cd may modulate brain cholinergic mechanism(s), neural excitability and metabolic energy production, and c) L-cysteine can have a protective antioxidant effect on the oxidative stress of the brain induced by Cd.     

Effects of ethanol administration on rat liver plasma membrane-bound enzymes

Changes in the properties of rat liver plasma membranes were examined in studies designed to differentiate between direct and metabolic effects of acute and chronic ethanol ingestion. One hour after a single dose of ethanol (3 g/kg body weight) there were increases in Na+,K+-ATPase (32%) and 5'-nucleotidase (36%), and hepatic concentrations of ethanol and acetaldehyde were approximately 23 mM and 50 microM, respectively. Na+,K+-ATPase and 5'-nucleotidase activities in liver plasma membranes from control rats were not significantly changed by in vitro addition of 30 microM acetaldehyde or 50 mM ethanol. Increases in Na+,K+-ATPase (approximately 20%) and 5'-nucleotidase (approximately 30%) were also observed in liver plasma membranes isolated from rats 16 hr after feeding ethanol or sucrose supplements for 17 days. The intake of calories from dietary protein and lipid was decreased by about 25% in both the ethanol and sucrose-fed animals. Na+,K+-ATPase activities in liver plasma membranes isolated from control rats were inhibited (approximately 20%) by 100 mM ethanol in vitro, whereas no inhibition was observed using membrane preparations from rats fed ethanol or sucrose supplements. Our results show that changes in liver plasma membrane enzyme activities associated with a single dose of ethanol are not a direct effect correlated with blood, hepatic or plasma membrane concentrations of ethanol or acetaldehyde. Chronic ingestion of ethanol or sucrose supplements had similar effects on liver plasma membrane enzyme characteristics and parallel changes in nutrient intake may be a more feasible explanation of these results than any analogous direct effects of the two compounds.