青龙衣多糖对H22型肿瘤细胞ATP酶活性的影响

目的：以H22肿瘤细胞为试验对象，采用体内试验，探讨青龙衣多糖是否可以影响ATP酶活性。方法：实验共设5个组，即阴性对照组（生理盐水组），阳性对照组（5-氟尿嘧啶组），青龙衣多糖低、中、高剂量组。整体水平观察青龙衣多糖的抑瘤和生命延长作用；按照测定无机磷含量的方法对H22肿瘤细胞的Ca^2＋-AT-Pase、Na^＋K^＋-ATPase和Mg^2＋-ATPase活性进行了测定；用荧光偏振法测定荧光偏振度值和微粘度研究细胞膜脂的流动性；采用化学比色法测定荷瘤小鼠H22肿瘤细胞的唾液酸含量。结果：青龙衣多糖高、中、低剂量组具有显著的抑瘤作用（P〈0．05），其中高剂量组抑瘤率达41．10％；同时青龙衣多糖具有明显的生命延长作用（P〈0．05），高剂量组生命延长率达75．00％。青龙衣多糖低、中、高剂量组可以抑制H22肿瘤细胞的Ca^2＋-ATPase的活性，抑制Mg^2＋-ATPase的活性；抑制降低H22肿瘤细胞膜的流动性；降低H22细胞膜表面唾液酸含量。结论：青龙衣多糖体内给药具有显著的抑瘤作用，显著抑制H22肿瘤细胞的ATP酶活性，影响其所转运的离子在细胞内外的空间分布。导致膜电位下降，物质转运受阻，细胞渗透压升高，细胞裂解，也可引起细胞凋亡容积下降，诱导凋亡的发生，膜流动性和唾液酸含量下降，可以影响ATP酶的结构活性和离子转运，这几方面的协调作用，可能是青龙衣多糖体内给药具有显著的抑瘤作用的机制之一。     

青龙衣多糖对S180小鼠红细胞内阳离子的影响

目的考察青龙衣多糖对S180小鼠红细胞内Ca^2＋和H^＋的影响。方法建立肿瘤动物模型，分高、中、低剂量腹腔给予青龙衣多糖7a。采集红细胞，制备红细胞悬液。应用激光扫描共聚焦显微镜结合荧光探针Fluo-3／AM染色观察和测定S160小鼠红细胞内Ca^2＋的变化．结合荧光探针BCECF—AM染色观察和测定S180小鼠红细胞内H＋的变化。结果青龙衣多糖能降低S180小鼠红细胞内Ca^2＋与阴性对照组相比较有显著性差异（P〈0.05）：青龙衣多糖各剂量组均能显著降低S180小鼠红细胞膜内的H^＋浓度，与阴性对照组相比较有显著性差异（P〈001）。结论青龙衣多糖组能维持S180小鼠红细胞内阳离子浓度稳定平衡。     

甲状腺机能减退征患者红细胞膜Ca2+.Mg2+ -ATPase活性测定

目的了解红细胞膜钙-镁三磷酸腺苷酶（Ca^2＋．Mg^2＋ -ATPase）活性在甲状腺功能减退征患者中的变化及该酶活性是否随甲状腺功能的恢复而逆转至正常,以确定该酶活性可否作为甲状腺激素在细胞水平作用的一个指标。方法低温、低渗溶解红细胞,差速离心法制备红细胞膜悬液。酶活性以含酶的红细胞膜悬液水解底物ATP释放出无机磷的量表示,无钙条件下无机磷的产生量为Mg^2＋ -ATPase活性。有钙条件下无机磷的产生量为总ATPase活性,二者之差为Ca^2＋．Mg^2＋ -ATPase活性。结果甲状腺功能减退患者红细胞Ca^2＋．Mg^2＋ -ATPase活性明显低于正常组。但3月后,随着甲状腺功能恢复正常,酶活性也随之恢复正常。结论红细胞膜Ca^2＋．Mg^2＋ -ATPase活性可作为甲状腺激素在细胞水平作用的一个指标,用于甲状腺功能异常的辅助诊断。     

利多卡因对家兔心肌缺血/再灌注损伤氧自由基及Na+-K+-ATPase、Ca2+-Mg2-ATPase的作用

目的观察利多卡因对心肌缺血再灌注损伤家兔血清GSH—P^2X、MDA及心肌组织Na^＋ - K^＋ - ATPase、Ca^2＋ - Mg^2＋ - ATPase的影响。方法24只家兔随机分为3组：假手术组（A组）、缺血／再灌注组（B组）、利多卡因组（c组），每组8只。B组、C组阻断左冠状动脉前降支40min．再灌注90min．A组仅穿线不结扎。C组于开放冠状动脉再灌注前经颈静脉注射利多卡因5mg／kg，B、C组注射等量生理盐水。于再灌注90min取颈静脉血测定GSH—PX、MDA;再灌注90min后取心肌组织测定Na^＋ - K^＋ - ATPase、Ca^2＋ - Mg^2＋ - ATPase。结果血清GSH—PXB组较A、C组降低（P〈0．01）、血清MDAB组较A、C组升高；心肌组织Na^＋ - K^＋ - ATPase、Ca^2＋ - Mg^2＋ - ATPase B组较A、C组降低（P〈0．01）。结论利多卡因对心肌缺血再灌注损伤具有保护作用。     

原发性高血压肾病患者红细胞ATP酶活性检测的临床意义

目的 探讨原发性高血压肾病患者红细胞膜Na^＋、K^＋-ATP酶活性的改变参与原发性高血压肾病的可能机制。方法 按Reilni制膜法测定32例原发性高血压无肾病和40例原发性高血压肾病患者红细胞膜Na^＋、K^＋-ATP酶和Ca^2＋、Mg^2＋-ATP酶含量,并与35名正常健康人作比较。结果 原发性高血压无肾病组和肾病组细胞膜Na^＋、K＋-ATP酶和Ca^2＋、Mg^2＋-ATP酶活性均显著地低于正常人组（P〈0.01）。原发性高血压肾病组与无肾病组亦有显著性差异（P〈0.05）。结论 原发性高血压肾病的发生和发展与细胞膜Na^＋、K^＋-ATP酶和Ca^2＋、Mg^2＋-ATP的活性有密切的关系。     

芦荟苷预处理对缺血再灌注大鼠心肌细胞凋亡、TNF-α含量和Ca2+-ATPase活性的影响

摘要：目的研究芦荟苷（Barbaloin,Barb）对急性心肌缺血再灌注损伤大鼠心肌细胞凋亡的影响。方法结扎大鼠左冠状动脉前降支复制心肌缺血再灌注损伤模型,实验分为假手术组、缺血再灌注组（IR）、Barb高、低剂量预处理组。采用原位缺口末端标记法（TUNEL）检测心肌细胞凋亡指数（AI）,ELISA法测定血清TNF—α水平,化学法测定线粒体Ca^2＋-ATPase活性。结果与IR组比较,Barb组AI和TNF-α水平显著降低（P〈0．05或P〈0．01）,Ca^2＋-ATPase活性明显增高（P〈0．05）。结论Barb能明显抑制IR引起的心肌细胞凋亡,其作用可能与降低TNF-α水平和提高Ca2＋-ATPase活性有关。     

铝对大鼠海马神经细胞线粒体酶的影响

目的探讨线粒体酶在铝致大鼠凋亡神经细胞中的改变。方法健康雄性SD大鼠40只，按体重随机分为4组：生理盐水、AL^3＋ 2．5、5、10mg／kg组。腹腔注射染毒60d后处死，用TUNEL法检测细胞凋亡，电镜观察线粒体结构的改变，用试剂盒测定线粒体超氧化物歧化酶（SOD），琥珀酸脱氢酶（SDH），三磷酸腺苷（ATP）酶（总ATP、Na^＋-K^＋ATP，Ca^2＋ ATP和Mg^2＋ ATP酶）活力。结果 随染铝剂量的增高，凋亡指数（AI）逐渐升高（P〈0．05），Na^＋-K^＋ ATP酶、Ca^2＋ ATP酶、Mg^2＋ ATP酶和SOD均降低（P〈0．05）；海马神经细胞SDH均数降低，但差异无显著性（P〉0．05）。海马神经细胞凋亡指数与Na^＋-K^＋ ATP酶、Ca^2＋ ATP酶、Mg^2＋ ATP酶和SOD呈负相关（r=-0．439，-0．501，-0．530，-0．815，P〈0．05），与SDH没有相关性（r=0．287，P〉0．05）。结论铝可以诱导大鼠海马神经细胞凋亡，并引起线粒体结构和线粒体酶活力的改变。     

羊栖菜多糖通过Ca^2＋影响S180荷瘤小鼠红细胞膜功能的研究

目的：从红细胞膜功能角度探讨羊栖菜多糖抗肿瘤作用机制，特别是红细胞内[Ca^2＋]的变化、膜电荷密度和膜电位变化。方法：实验共设6组。体内抑瘤实验和生命延长实验；激光共聚焦测定荷瘤小鼠红细胞内[Ca^2＋]的变化，分光光度法对荷瘤小鼠红细胞脆性的变化和唾液酸含量进行测定，结合高效毛细管电泳法对荷瘤小鼠红细胞电泳淌度的测定结果，探讨荷瘤小鼠红细胞膜表面电荷密度的变化情况；用荧光偏振法测定荧光偏振度值和微粘度研究细胞膜脂的流动性；按Zamudio法进行NADH-细胞色素C氧化还原酶活性的测定，计算荷瘤小鼠红细胞的封闭度；测定荷瘤小鼠红细胞膜Na＋，K＋-ATPase及Ca2＋，Mg2＋-ATPase活性，用流式细胞仪测量荷瘤小鼠红细胞膜膜电位的变化趋势。结果：（1）羊栖菜多糖能够抑制S180荷瘤小鼠的肿瘤生长和延长H22荷瘤小鼠的生存时间；（2）羊栖菜多糖能够降低S180荷瘤小鼠红细胞内[Ca2＋]、红细胞脆性，提高S180荷瘤小鼠红细胞膜流动性和封闭度；（3）羊栖菜多糖能够提高S180荷瘤小鼠红细胞膜表面的唾液酸含量、Na＋，K＋-ATPase及ca2＋，Mg2＋-ATPase活性；（4）羊栖菜多糖能够提高S180荷瘤小鼠红细胞膜膜电位水平和红细胞表面的电泳淌度，即增加表面的电荷密度。结论：羊栖菜多糖能提高荷瘤小鼠红细胞膜功能，增强红细胞免疫功能，通过对体内循环复合物的免疫粘附作用，达到抗肿瘤效果，这可能是羊栖菜多糖抗肿瘤作用机制之一。     

Ⅱ型糖尿病肾病和红细胞膜ATP酶活性的关系

目的 探讨Ⅱ型糖尿病患红细胞膜Na^K^ -ATP酶和Ca^2 Mg^2 -ATP酶活性改变参与糖尿病肾病的可能机制。方法 按Reinila制膜法测定了25例无糖尿病肾病和57例糖尿病肾病患红细胞膜Na^ K^ -ATP酶和Ca^2 Mg^2 -ATP酶含量,并与35名正常人作对照。结果 糖尿病无肾病组和肾病组红细胞膜Na^ -K^ -ATP酶和Ca^2 Mg^2 -ATP酶活性均显地低于正常人组（P＜0．01）,糖尿病肾病组与无肾病组比较差异亦有显性（P＜0．05）。结论 Ⅱ型糖尿病肾病的发生和发展与红细胞膜Na^2 K^ -ATP酶和Ca^2 Mg^2 -ATP酶活性有密切的关系。     

西兰花中葡萄糖异硫氰酸盐诱导肿瘤细胞凋亡作用及机理研究

目的：探讨西兰花中葡萄糖异硫氰酸盐体内、体外抗肿瘤作用，并初步探讨作用机理。结果：在体内研究中，实验以S180和H22小鼠为研究对象。实验结果表明，GS对S180／小鼠具有抑瘤作用，其中，以中、高剂量组效果最好，与阴性对照组相比具有显著性差异（P〈0.01），抑瘤率呈现一定量效关系（45.45％、57.58％、63.64％）；在生存时间方面，GS能延长H22小鼠的生存时间，其中以高剂量的生存时间延长显著（P〈0．05）。GS还能升高S180小鼠胸腺指数和脾指数，与阴性组比较有显著性差异（P〈0．05，P〈0.01），说明GS对荷瘤小鼠两大免疫器官具有良好的保护作用。在体内抗肿瘤研究中。GS可提高S180和H22小鼠红细胞中SOD、CAT和全血中GSH的活性，并降低全血中红细胞MDA含量。GS的抗肿瘤作用可能是通过提高SOD、CAT、GSH活性，和降低自由基水平来实现的。在体外研究中GS对SGC-7901和HepG2细胞的凋亡过程及其可能机理。从SRB实验结果可看出，1、10、100和1000μg／mL的GS作用于SGC-7901和HepG2细胞72h后，均可抑制肿瘤细胞的增殖，采用荧光倒置显微镜观察GS作用于SGC-7901和HepG2细胞18h后，细胞均出现早期凋亡细胞的形态；通过流式细胞仪检测得300、600、1200μg／mL的GS作用于SGC-7901和HepG2细胞18h后，SGC-7901细胞凋亡率分别为14．544％、10．110％、34．117％，对细胞周期作用显著；HepG2细胞凋亡率分别为2．159％、16．538％和54．455％。可见GS具有一定程度诱导肿瘤细胞凋亡的作用。在GS诱导肿瘤细胞凋亡机理实验中，300、600、1200％μg／mL的GS作用于SGC-7901和HepG2细胞18h后，肿瘤细胞内的Ca^2＋。浓度剂量升高，此作用可能是GS诱导肿瘤细胞凋亡的作用机理之一。线粒体是细胞凋亡的调控中心。所以，通过流式细胞仪检测300、600、1200μg／mL的GS作用于SGC-7901和HepG2细胞18h后，肿瘤细胞内活性氧均增加，线粒体跨膜电位均降低。GS诱导肿瘤细胞凋亡可能是Ca^2＋、活性氧和线粒体之间相互作用的结果，这也许是GS诱导肿瘤细胞凋亡的机理之一。结论：GS无论在体内还是在体外研究中均表现出良好的肿瘤抑制作用，具有一定的诱导肿瘤细胞凋亡的作用。     

心脑宁片对脑缺血大鼠乳酸、LDH、ATP酶活力的影响

目的 研究心脑宁片对大鼠脑缺血模型脑匀浆乳酸(lactic acid,LD)、乳酸脱氢酶(lactate dehydrogenase,LDH)水平及三磷酸腺苷(adenosine-triphosphate,ATP)酶活力的影响。方法 Wistar大鼠随机分为7组,每组12只：空白对照组,高、中、低剂量心脑宁片组、尼莫地平组、脑安片组和羧甲基纤维素钠组,测定脑匀浆中蛋白含量、LD、LDH、ATP酶水平。结果 大鼠脑缺血模型造模成功。与模型组相比,各剂量心脑宁片均可显著降低脑匀浆LD水平(P<0.01),升高脑匀浆LDH活力(P<0.01),并可显著升高脑匀浆Na⁺-K⁺-ATPase(P<0.01)、Mg²⁺-ATPase和Ca²⁺-ATPase活力(P<0.01或P<0.05)结论 心脑宁片具有明显改善脑缺血作用。     

Adenosine triphosphatase activities in plasma liver membranes of rats treated with DDT and toxaphene

The effect of exposure to chlorinated insecticides (DDT and toxaphene) on Na+,K+-ATPase, Mg2+-ATPase and Ca2+-ATPase activities of the plasma membrane of hepatocytes was determined. Acute treatment with DDT (200 mg per kg body weight) or toxaphene (110 mg per kg body weight) produced a significant decrease in Na+,K+-ATPase activity (80% and 85%, respectively) 24 h after treatment. DDT also produced a 30% decrease in Mg2+-ATPase and Ca2+-ATPase activity, but toxaphene treatment did not modify these enzymes. The effect of exposure to daily doses of DDT (30 mg per kg body weight) or toxaphene (16.5 mg per kg body weight) for a period of 3.5 months was also studied. Animals were sacrificed at 15-day intervals and results showed that Na+,K+-ATPase activity decreased 80% from the beginning of each treatment and the activity remained low throughout the treatment period. DDT, but not toxaphene, also led to a decrease in Mg2+-ATPase (20%) and Ca2+-ATPase (35%) activity. The low values observed from the beginning remained low throughout the treatment period. We believe that the general mechanism of ATPase inhibition by organochloride compounds could be the result of its interaction with membrane lipid components, although some differences could arise from differences in their spatial structure.     

Contribution of lipid dynamics on the inhibition of bovine brain synaptosomal Na+-K+-ATPase activity induced by 4-hydroxy-2-nonenal

The effects of lipid hydroperoxide degradation products, such as 4-hydroxy-2-nonenal (HNE) and malondialdehyde (MDA), on bovine brain synaptosomal ATPase activities and their membrane lipid organization were examined. When the synaptosomes were treated with HNE, this resulted in the decrease of Na(+)-K(+)-ATPase activity with the loss of sulfhydryl (SH) groups in the membrane proteins. In contrast, MDA treatment of the synaptosomes did not induce an appreciable decrease in the ATPase activity or a loss of SH groups. The decreases in ATPase activity and SH content by treatment with HNE were also observed, as a Na+-K+-ATPase preparation was used in place of the synaptosomes. On the other hand, HNE had very little effect on synaptosomal Ca2+- and Mg2+-ATPase activities. The results of the kinetic analysis of the Na+-K+-ATPase activity indicated that the decrease in the activity by HNE-modification is due to a decreased affinity for the substrate. ATP completely protected the ATPase from the HNE attack. Modification of the synaptosomes with HNE caused a decrease in the membrane lipid fluidity near the lipid/water interface, not the lipid layer interior. In addition, it was found that there is a good relationship between the lipid fluidity and the Na+-K+-ATPase activity under the presence of various concentrations of HNE, suggesting that the lipid dynamics are closely related to HNE-induced inhibition of the ATPase activity. On the other hand, MDA did not induce change in the membrane lipid fluidity. HNE and MDA are mainly incorporated into the lipid and protein fractions in the synaptosomal membranes, respectively. Based on these results, we proposed a possible mechanism of HNE-induced inhibition of synaptosomal Na+-K+-ATPase activity associated with alterations in the membrane lipid organization.     

香烟烟雾染毒对雄性大鼠睾丸组织 ATP 酶活性的影响

目的 探讨香烟烟雾染毒对大鼠睾丸结构及睾丸组织 ATP 酶活性的影响。方法 清洁级成年雄性 SD 大 鼠 70 只, 随机分为对照组 （10 只） 和低、 中、 高剂量染毒组 （每组 20 只, 分别给予 10 支、 20 支、 30 支香烟烟雾暴露）。 染毒组采用呼吸道静式染毒, 每日 1 次, 每次 30 min, 各剂量染毒组分别染毒 6 周和 12 周（每个时段 10 只大鼠）。 实验期间记录各组大鼠体质量变化。实验结束后, 摘取睾丸, HE 染色观察睾丸组织结构, 酶联免疫吸附试验检测睾 丸组织 Na＋-K＋-ATP 酶、 Ca２＋-ATP 酶活性。结果 随染毒剂量增加, 各组大鼠体质量逐渐降低 （P < 0.05）。染毒组 大鼠睾丸病理切片观察到不同程度损伤, 且随着染毒时间的延长和染毒剂量的增加, 损伤逐渐加重。染毒 6 周后, 高剂量组大鼠睾丸组织 Na+-K+-ATP 酶活性低于其他 3 组 （P < 0.05）, Ca2+-ATP 酶活性低于对照组 （P＜0.05）。染毒 12 周后, 低、 中、 高剂量组大鼠睾丸组织 Na+-K+-ATP 酶、 Ca2+-ATP 酶活性均较对照组显著降低（P < 0.05）。结论 香烟烟雾染毒可减缓雄性大鼠生长, 导致睾丸组织损伤, Na+-K+-ATP 酶和 Ca2+-ATP 酶活性降低。     

Influence of alpha 1-adrenergic receptor stimulation and phorbol esters on hepatic Na+/K+-ATPase activity

The effects of the alpha 1-adrenergic agonist phenylephrine (PE) and the phorbol ester 4 beta-phorbolmyristate-acetate (PMA) on sodium pump function were studied in the rat liver. In order to distinguish between direct and indirect influences, ouabain-sensitive 86Rb uptake by intact liver slices was compared with ouabain-sensitive Na+/K+-ATPase activity in plasma membranes isolated from PE and PMA-perfused livers. At a buffer Ca2+ level of 2.5 mmol/l, PE (10 mumol/l) caused an initial stimulation of both 86Rb uptake and Na+/K+-ATPase activity followed at 5 min by a decrease in both activities. Both actions were blocked by the alpha 1-antagonist prazosin. The decrease in ouabain-sensitive Na+/K+-ATPase was paralleled by an increase in Mg2+ ATPase activity. At a Ca2+ level of 1.5 mmol/l, PE stimulation of 86Rb uptake and Na+/K+-ATPase was sustained, and the inhibitory component was not expressed. PMA (4 mumol/l) reduced 86Rb uptake and Na+/K+-ATPase and similar to PE, this inhibition was paralleled by an increase of Mg2+-ATPase activity. 4 alpha-PMA, which does not activate protein kinase C, failed to influence 86Rb uptake or Na+/K+-ATPase. These results demonstrate that PE and PMA effects on ouabain-sensitive 86Rb uptake are preserved in isolated membranes, indicating a direct influence on the Na+/K+-ATPase. A role for protein kinase C in modulating sodium pump activity is suggested.     

川芎嗪对大鼠加速型抗GBM抗体肾炎肾皮质的线粒体膜流动性和ATP酶活性的影响

目的 观察川芎嗪对大鼠加速型抗肾小球基底膜(GBM)抗体肾炎肾皮质线粒体膜流动性和ATP酶活性的影响。方法采用1,6-二苯基-1,3,5-己三烯(DPH)荧光偏振法研究抗GBM肾炎肾皮质的线粒体膜流动性,利用定磷法测定线粒体膜ATP酶的活性。结果川芎嗪能调节抗GBM抗体肾炎肾皮质的线粒体膜流动性,同时可以使Na^ -K^ -ATPase、Mg^ -ATPase、Ca^2 -ATPase活力升高。结论川芎嗪可能通过改善肾线粒体膜流动性,而保护线粒体膜结构及功能。     

Effect of hydroxychlorodiphenyl ethers (chlorinated pre-and isopredioxins) on erythrocyte membrane adenosinetriphosphatase activity

The effect of hydroxychlorodiphenyl ethers (HO-ClX-DPEs; chlorinated pre- and isopredibenzodioxins), contaminants of technical chlorophenol preparations, on human erythrocyte membrane-bound adenosinetriphosphatases (ATPases) has been investigated. Both 2- and 3-HO-Cl9-DPE inhibited the Na+ + K+-activated, Mg2+-dependent ATPase (Na+, K+, Mg2+-ATPase). The Mg2+-dependent ATPase (Mg2+-ATPase) was stimulated at lower concentration of these compounds, but at higher concentrations there was a gradual decrease in the extent of stimulation, 2-Hydroxy-21, 41, 41-trichlorodiphenyl ether (2-HO-Cl3-DPE; Irgasan DP-300; Triclosan) was not as effective as the nonachloro compounds at inhibiting Na+, K+, Mg2+-ATPase and was inactive at stimulating Mg2+-ATPase. Pure pentachlorophenol (PCP) caused both inhibition of Na+, K+, Mg2+-ATPase and stimulation of Mg2+-ATPase, although each effect required a higher concentration of PCP than was needed for the HO-CL9-DPEs. The possible relationship of the effects of HO-CL x-DPEs on human erythrocyte membrane ATPase activities to the potent hemolytic activity of these compounds is discussed.     

大蒜新素对肾型高血压大鼠和老年大鼠脑皮质微粒体ATPase活力的影响

目的研究大蒜新素（ａｌｌｉｔｒｉｄｉ,Ａｌｌ）对肾型高血压大鼠和老年大鼠脑皮质微粒体ＡＴＰａｓｅ活力的影响。方法用两肾一夹法建立大鼠Ｇｏｌｄｂｌａｔｔ肾型高血压模型;以钼酸铵定磷,采用光电比色法测定ＡＴＰａｓｅ活力。结果肾型高血压大鼠和老年大鼠中,脑皮质微粒体中Ｎａ＋,Ｋ＋－ＡＴＰａｓｅ和Ｃａ２＋,Ｍｇ２＋－ＡＴＰａｓｅ活力比成年大鼠中显著降低,Ｍｇ２＋ＡＴＰａｓｅ无明显改变。大蒜新素（１５ ｍｇ·ｋｇ．ｄ－ｌ ｉｇ, ６０ ｄ）可显著提高肾型高血压大鼠和老年大鼠脑皮质微粒体中Ｎａ＋,Ｋ＋－ＡＴＰａｓｅ和Ｃａ２＋,Ｍｇ２＋－ＡＴＰａｓｅ活力,而对Ｍｇ２＋－ＡＴＰａｓｅ无明显影响。结论大蒜新素对大鼠脑皮质微粒体的Ｎａ＋,Ｋ＋－ＡＴＰａｓｅ和Ｃａ２＋,Ｍｇ２＋－ＡＴＰａｓｅ活力的提高可能有利于大蒜新素防治脑缺血作用。     

Calmodulin-stimulated plasma membrane (Ca2+ + Mg2+)-ATPase: inhibition by calcium channel entry blockers

Calcium channel entry blockers representing different structural classes were studied for their effects on human erythrocyte basal and calmodulin-stimulated (Ca2+ + Mg2+)-ATPase. Effects on the activity of (Mg2+)-ATPase and (Na+ + K+)-ATPase were also assessed. Of the four Ca2+ entry blockers tested, only verapamil and diltiazem specifically inhibited the calmodulin-stimulated (Ca2+ + Mg2+)-ATPase activity, the basal enzyme activity being unaltered by these drugs. Other membrane-associated ATPases were not affected. Calmodulin concentration effect curves showed the inhibition by verapamil (10(-3) M) and diltiazem (10(-3) M) to be non-competitive. This concentration inhibited the calmodulin-dependent increment (5.1 nM calmodulin) of the ATPase activity by 35 and 36% respectively. Similarly, both drugs inhibited the Ca2+-activation process of calmodulin-stimulated activity in a non-competitive manner, decreasing Vmax by 23 and 17% respectively. Basal (Ca2+ + Mg2+)-ATPase activity was not affected by verapamil or diltiazem at any calcium concentration. In contrast, cinnarizine non-specifically inhibited all four membrane ATPases including calmodulin-stimulated (Ca2+ + Mg2+)-ATPase activity at concentrations above 3 X 10(-6) M. Nifedipine was without effect on any of the four membrane ATPases. From this we conclude that certain calcium channel entry blockers can inhibit calmodulin-regulated plasma membrane Ca2+-pump ATPase. Therefore, this identifies an additional functional low affinity receptor in the plasma membrane for some of the calcium channel entry blockers.     

牛磺酸对2型糖尿病大鼠胰腺线粒体氧化应激的影响

目的探讨牛磺酸对糖尿病大鼠胰腺线粒体氧化应激的影响。方法将30只Wistar大鼠随机分为正常对照组、糖尿病组(DM组)和牛磺酸治疗组(Tau组,采用20g.L-1牛磺酸生理盐水溶液治疗,200mg·kg-1),前两组注射等体积的生理盐水溶液。8wk后,测3组大鼠血浆葡萄糖、胰岛素、丙二醛(MDA),胰腺线粒体MDA、Ca2+、超氧化物歧化酶(SOD)及Na+,K+-ATP酶(Na+,K+-ATPase)和Ca2+,Mg2+-ATP酶(Ca2+,Mg2+-ATPase)的活性。结果①DM组大鼠血糖、MDA和胰腺线粒体MDA、Ca2+含量明显高于对照组(P<0.01),而血浆胰岛素水平、SOD、Na+,K+-AT-Pase和Ca2+,Mg2+-ATPase活性明显降低(P<0.05)。②Tau组大鼠血糖、MDA及胰腺线粒体Ca2+、MDA含量较DM组明显降低(P<0.05),血浆胰岛素水平、SOD、Na+,K+-ATPase和Ca2+,Mg2+-ATPase活性明显升高(P<0.05)。结论牛磺酸可减轻2型糖尿病大鼠胰腺线粒体氧化应激水平。