共查询到20条相似文献,搜索用时 15 毫秒
1.
实验将16只新西兰兔随机分为4组,由耳缘静脉注射被试物:1-NS(0-9%NaCl1mLkg);2-Tau(3mmolkg);3-ET(100EUkg);4.ET(100EUkg)+Tau(3mmolkg)。在注射后4h从颈动脉取血,离心取血清,用原子分光光度法检测血清Fe2+、Zn2+、Cu2+含量结果见表1:表1 4组家兔血清Fe2+、Zn2+、Cu2+含量(mgL,珋x±s,n=4)GroupFe2+Zn2+Cu2+NS3-61±0-771-22±0-550-57±0-17Ta… 相似文献
2.
目的观察旱黑口服液对D-gal衰老小鼠心肌细胞膜、脑细胞膜上Na -K -ATP,ase、Ca2 -Mg2 -ATPase活性的影响,探讨旱黑口服液在延缓衰老方面的效应机制。方法以D-gal致亚急性衰老小鼠为模型,同时给予旱黑口服液治疗,6周后测定心、脑细胞膜上Na -K -ATPase、Ca2 -ATPase活性。结果与空白组比较,衰老组心、脑细胞膜上Na -K -ATPase、Ca2 -Mg2 -ATPase活性降低,经旱黑口服液治疗后心、脑细胞膜上Na -K -ATPase、Ca2 -Mg2 -ATPase活性活性明显提高。结论旱黑口服液具有提高D-gal致衰老小鼠心、脑细胞膜上Na -K -ATPase、Ca2 -Mg2 -ATPase活性,延缓衰老的作用。 相似文献
3.
Anant B. Parekh 《Pflügers Archiv : European journal of physiology》1995,430(6):954-963
The relationship between capacitative Ca2+ influx and activation of Ca2+-dependent Cl– channels was monitored in intactXenopus oocytes following stimulation of 5-hydroxytryptamine (5-HT) receptors, through the activity of Ca2+-dependent Cl– channels using the double-electrode voltage-clamp technique. Under voltage-clamp conditions, 5-HT evoked a rapid transient inward current followed by a slowly developing secondary inward current. The secondary current reflected depletion-activated Ca2+ entry. Hyperpolarising pulses evoked sustained Ca2+-dependent Cl– currents when applied during the transient inward current, but evoked hump-like currents which inactivated rapidly when applied during the secondary inward current. Hump currents arose from Ca2+ entering through the depletion-activated pathway. The hump currents inactivated with hyperpolarising pulses at <5-s intervals, and recovered monoexponentially with a time constant of around 8 s. Currents in response to hyperpolarising pulses during the transient current did not inactivate, suggesting that inactivation was associated with Ca2+ entry. When Ca2+ release evoked by inositol 1,4,5-triphosphate [Ins(1,4,5)P
3] was prevented by heparin injection, hyperpolarising pulses during Ca2+ ionophore application also generated hump currents that were dependent on external Ca2+, inactivated and recovered from inactivation with a similar time course as the humps following 5-HT treatment. Pretreatment with the Ca2+ adenosine 5-triphosphatase (Ca2+ATPase) inhibitor thapsigargin reduced the rate of rise of the hump current, increased the time-to-peak of the current and slowed the rate of decay. Pharmacological interventions to disrupt the cytoskeleton reduced the amplitude of the hump current. It is suggested that, following hyperpolarisation in the presence of Ca2+ entry, the ensuing Ca2+ influx interacts with Cl– channels in a way that might reflect both Ca2+ inhibition of Ca2+ entry and clustering of Cl– channels in the plasma membrane. 相似文献
4.
王静 《国际病理科学与临床杂志》2012,32(5)
许多心血管疾病如原发性高血压的发生和发展,均与血管内皮细胞结构的损伤和功能异常有密切关系.而血管内皮细胞的损伤,一方面可以导致一氧化氮(nitric oxide,NO)合成减少及分泌异常,另一方面也使细胞膜对钙离子处理异常.NO和Ca2+可通过各自和两者之间的相互作用对原发性高血压的发生和发展起到重要的调控作用. 相似文献
5.
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 总被引:9,自引:1,他引:8
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8783%、Ca2+-Mg2+-ATP酶和Ca2+-ATP酶活性分别降低3756%和5020%(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=-079,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。 相似文献
6.
目的 :研究ClC - 3Cl-通道在培养的牛脑血管平滑肌细胞 (CSMC)Ca2 + 池操纵性Ca2 + 内流中的作用。方法 :采用培养的CSMC ,用硫代磷酸修饰的ClC - 3反义寡核苷酸与脂质体一起转染入平滑肌细胞 4 8h ,以正义和随机序列寡核苷酸作为对照 ,在生物荧光双波长影像分析系统用Fura- 2 /Am荧光探针测定单个细胞内游离Ca2 + 浓度。结果 :(1)采用Ca2 + ImageSystem测定脑血管平滑肌细胞静息 [Ca2 + ]i ,以 340 / 380nm波长的比值表示为 0 6 84± 0 0 0 2 ,内皮素 - 1(ET - 1) 10 -7mol·L-1刺激细胞引起 [Ca2 + ]i呈双相升高反应 ,先是快… 相似文献
7.
目的:探讨房颤时心房肌细胞膜上L型Ca2+通道与肌浆网之间的Ca2+信号转导。 方法: 杂种犬10条,随机分为正常对照组和单纯房颤组。房颤组用起搏器行右心房快速起搏(500±20)次/分,术后观测24周。正常对照组不植入起搏器。胶原酶Ⅱ型分离心房肌细胞,用激光共聚焦显微镜检测L型Ca2+ 通道对细胞内Ca2+浓度变化的影响;L型Ca2+通道与肌浆网三磷酸肌醇受体(IP3R)和兰尼碱受体(RyR)之间的Ca2+信号转导。 结果: (1)L型Ca2+通道与肌浆网IP3R之间的Ca2+信号转导:正常对照组、单纯房颤组的心房肌细胞在用mibefradil和丁卡因分别阻滞T型Ca2+通道和RyR后给予细胞膜激动剂时,细胞内Ca2+浓度均升高(分别为1.4000±0.0776和1.5169±0.4414),组间比较无显著差异(P>0.05);(2)L型Ca2+通道与肌浆网RyR之间的Ca2+信号转导:正常对照组的心房肌细胞在用mibefradil和肝素分别阻滞T型Ca2+通道和IP3R后给予细胞膜激动剂时,细胞内Ca2+浓度升高(1.5576±0.1989),单纯房颤组的细胞内Ca2+浓度也升高(1.5372±0.2952),两组间比较无显著差异(P>0.05)。 结论: 房颤时L型Ca2+通道与RyR和IP3R之间可能存在信号转导,但其可能在房颤时的细胞内Ca2+超载及异常Ca2+信号转导方面不起重要作用。 相似文献
8.
阿片受体包括κ ,μ ,δ等多种亚型 ,属G蛋白偶联受体 ,广泛分布于神经系统。阿片受体可通过与神经细胞内第二信使Ca2 + 偶联 ,调节神经细胞的功能。κ ,δ阿片受体被激活后对神经细胞Ca2 + 通道的作用存在双向性 ,即通过多种途径或不同方式 ,抑制或激活Ca2 + 通道。δ阿片受体激活后可动员细胞内钙库 ,引起钙库释放增加 ;在多种神经细胞上 ,μ阿片受体激活后可抑制高电压依赖钙通道 ,而对低电压钙通道无明显影响。 相似文献
9.
T. M. Piser R. A. Lampe R. A. Keith S. A. Thayer 《Pflügers Archiv : European journal of physiology》1994,426(3-4):214-220
Field-potential stimulation of rat dorsal-root ganglion (DRG) neurons evoked action-potential-mediated transient increases in intracellular free calcium concentration ([Ca2+]i) as measured by indo-1-based microfluorimetry. Field-potential-evoked [Ca2+]i transients were abolished by tetrodotoxin, and their dependence on stimulus intensity exhibited an abrupt threshold. -Conotoxin GVIA (-CgTx, 100 nM) inhibited action-potential-mediated Ca2+ influx by 79%, while nitrendipine (1 M) had little effect. -Grammotoxin SIA (-GsTx, 267 nM), a peptide toxin purified from the venom of the tarantula spider, Grammostola spatulata, blocked action-potential-mediated Ca2+ influx as effectively as did -CgTx, suggesting that -GsTx blocks N-type Ca2+ channels. In contrast to block by -CgTx, the block produced by -GsTx reversed upon washout of the peptide. -GsTx (270 nM) blocked 80%, and -CgTx (1 M) blocked 64%, of whole-cell Ca2+ current (I
Ca) elicited by step depolarization to 0 mV from a holding potential of –80 mV. -GsTx completely occluded inhibition of I
Ca by -CgTx. However, when applied after -CgTx, -GsTx produced an additional inhibition of 27%, indicating that -GsTx also blocked a non-N-type Ca2+ channel. BayK8644 (1 M) elicited an increase in I
Ca in the presence of maximally effective concentrations of -GsTx, suggesting that -GsTx does not block L-type channels. Thus, -GsTx displays a selectivity for Ca2+ channel subtypes which should prove useful for studying Ca2+ channels and Ca2+-channel-mediated processes. 相似文献
10.
溶血磷脂酸对大鼠心肌细胞膜Na+-Ca2+交换的影响 总被引:4,自引:0,他引:4
本研究采用蔗糖梯度离心法制各大鼠心肌细胞膜,观察溶血磷脂酸( LPA)对心肌细胞膜 Na~+-Ca~(2+)交换的影 响。结果发现LPA(1~20nmol/L)呈剂量依赖性和时间依赖性刺激Na~+一Ca~(2+)交换活性增加。Gpp(NH)p呈剂量依赖 性替代LPA刺激的Na~+-Ca~(2+)交换活性;PTX可抑制LPA对Na~+-Ca~(2+)交换的激活;Genistein,Propranolol,Prazosin,Atropine,Losartan,BQ123和磷脂酰胆碱对LPA诱导的Na~+-Ca~2+交换活性无影响,而磷脂酰丝氨酸可增加对照和LPA 两组的 Na~+-Ca~(2+)交换活性。这些结果表明 LPA可通过 PTX敏感的 G蛋白刺激大鼠心肌细胞膜 Na~+-Ca~(2+)交换活性。 相似文献
11.
目的探讨外周血CD8~+CD25~+Foxp3~+Treg(CD8~+Treg)细胞比例在2型糖尿病(T2DM)疾病过程中的作用。方法选取T2DM患者90例。根据尿微量白蛋白(MAL),分为45例T2DM伴正常蛋白尿患者(NMAU,MAL30 mg/24 h),45例T2DM伴微量蛋白尿患者(MAU,MAL 30~300 mg/24 h),同时选择门诊体检健康人员45名作为对照组(HC)。通过特定蛋白仪检测患者mAlb浓度;流式细胞仪检测CD8~+Treg细胞比例;Luminex200检测血浆白细胞介素(IL)-8、1β、6和肿瘤坏死因子(TNF)-α浓度。结果与HC组[4.43(3.26~5.75)%]相比,NMAU组[4.06(3.15~5.43)%]和MAU组[3.52(2.30~4.87)%]患者CD8~+Treg细胞比例降低,且MAU组降低更明显(P0.05);与HC组相比,MAU组和NMAU组患者血浆细胞因子TNF-α、IL-8、IL-6和IL-1β浓度均升高(P0.05);MAU组患者CD8~+Treg比例与血清细胞因子TNF-α(r=-0.444 8,P0.01)、IL-8(r=-0.341 2,P0.05)、IL-6(r=-0.365 3,P0.05)和IL-1β(r=-0.319 2,P0.05)呈负相关;Logistic回归分析显示CD8~+Treg对T2DM患者可能具有保护作用。结论通过调控T2DM患者外周血CD8~+Treg细胞比例,有可能减缓糖尿病的进程。 相似文献
12.
Carlos B. Duarte Ildete L. Ferreira Arsélio P. Carvalho Caetana M. Carvalho 《Pflügers Archiv : European journal of physiology》1993,423(3-4):314-323
The specific inhibitor of the -aminobutyric acid (GABA) carrier, NNC-711, {1-[(2-diphenylmethylene) amino]oxyethyl}-1,2,5,6-tetrahydro-3-pyridinecarboxylic acid hydrochloride, blocks the Ca2+-independent release of [3H]GABA from rat brain synaptosomes induced by 50 mM K+ depolarization. Thus, in the presence of this inhibitor, it was possible to study the Ca2+-dependent release of [3H]GABA in the total absence of carrier-mediated release. Reversal of the Na+/Ca2+ exchanger was used to increase the intracellular free Ca2+ concentration ([Ca2+]i) to test whether an increase in [Ca2+]i alone is sufficient to induce exocytosis in the absence of depolarization. We found that the [Ca2+]i may rise to values above 400 nM, as a result of Na+/Ca2+ exchange, without inducing release of [3H]GABA, but subsequent K+ depolarization immediately induced [3H]GABA release. Thus, a rise of only a few nanomolar Ca2+ in the cytoplasm induced by 50 mM K+ depolarization, after loading the synaptosomes with Ca2+ by Na+/Ca2+ exchange, induced exocytotic [3H]GABA release, whereas the rise in cytoplasmic [Ca2+] caused by reversal of the Na+/Ca2+ exchanger was insufficient to induce exocytosis, although the value for [Ca2+]i attained was higher than that required for exocytosis induced by K+ depolarization. The voltage-dependent Ca2+ entry due to K+ depolarization, after maximal Ca2+ loading of the synaptosomes by Na+/Ca2+ exchange, and the consequent [3H]GABA release could be blocked by 50 M verapamil. Although preloading the synaptosomes with Ca2+ by Na+/Ca2+ exchange did not cause [3H]GABA release under any conditions studied, the rise in cytoplasmic [Ca2+] due to Na+/Ca2+ exchange increased the sensitivity to external Ca2+ of the exocytotic release of [3H]GABA induced by subsequent K+ depolarization. Thus, our results show that the vesicular release of [3H]GABA is rather insensitive to bulk cytoplasmic [Ca2+] and are compatible with the view that GABA exocytosis is triggered very effectively by Ca2+ entry through Ca2+ channels near the active zones. 相似文献
13.
14.
Ca2+与内质网途径的细胞凋亡 总被引:3,自引:0,他引:3
细胞Ca2+稳态的维持主要是通过内质网进行的,Ca2+在细胞内的活动多与内质网有关,胞内\[Ca2+\]的变化可以引起内质网应激,而过度的内质网应激则会导致细胞的凋亡。由于内质网和线粒体在细胞内空间结构上的接近,内质网释放的Ca2+又会引起线粒体途径的凋亡。一些内质网相关的因素也参与Ca2+所引起的细胞内质网途径的凋亡。 相似文献
15.
目的: 研究PAR-2激动剂对人肝癌HepG2细胞增殖及细胞内Ca2+浓度([Ca2+]c)的影响。方法: 培养人肝癌细胞HepG2, 分别利用PAR-2激动剂SLIGKV-NH2及反PAR-2激动肽VKGILS-NH2干预肝癌细胞生长,用Fura-2荧光法测定肝癌细胞内[Ca2+]c,用MTT法检测对肝癌细胞增殖能力的影响,流式细胞术(FCM)检测细胞周期改变情况,RT-PCR法检测cyclinD1 mRNA表达变化。结果: 50 μmol/L SLIGKV-NH2刺激HepG2细胞后,[Ca2+]c迅速短暂升高(P<0.01);G0/G1期比例明显降低,S期和G2/M期细胞比例和细胞增殖指数(PI)明显提高(P<0.01);cyclinD1 mRNA的表达显著增加(P<0.01)。SLIGKV-NH2在1-50 μmol/L时可以促进HepG2细胞增殖,呈剂量依赖性(P<0.01或P<0.05)。而VKGILS-NH2组与对照组相比差异无显著(P>0.05)。结论: PAR-2激动剂在体外能通过激活PAR-2,诱导HepG2细胞内[Ca2+]c升高,上调cyclinD1 mRNA的表达,加速HepG2细胞周期进程,促进DNA合成,促进肝癌细胞增殖。 相似文献
16.
目的:对最常用心脏血管替代材料涤纶片作最新发展的具有全方位表面改性特征的混合等离子体浸没注入,以观察经处理后的涤纶片抑制细菌粘附的效果.方法:用多功能全方位等离子体浸没及离子注入机(PIII),用射频电源建立气体等离子体,对涤纶材料作全方位乙炔和氩气混合离子(C2H+Ar)注入获取表面改性涤纶片.用金黄色葡萄球菌,表皮葡萄球菌,大肠杆菌,绿脓杆菌,白色念珠菌制取细菌悬液并作5-125Ⅰ-2′-脱氧尿嘧啶核苷(125Ⅰ-UDR)标记,再对改性涤纶材料作体外细菌动态粘附实验.结果:表面改性涤纶材料改变了亲水性和表面能,降低了水分子接触角.与未改性材料相比,改性涤纶材料抗细菌粘附能力有较明显提高.结论:混合离子(C2H2+Ar)表面改性涤纶片有良好的抗细菌和血小板粘附能力. 相似文献
17.
18.
Makoto Takano Frances M. Ashcroft 《Pflügers Archiv : European journal of physiology》1996,431(4):625-631
We studied the block of whole-cell ATP-sensitive K+ (KATP) currents in mouse pancreatic-cells produced by external Ba2+. Ba2+ produced a time- and voltage-dependent block of KATP currents, both the rate and extent of the block increasing with hyperpolarization. With 5.6 mM [K+]o, the relationship between the steady-state KATP current and [Ba2+]o, was fit by the Hill equation with aK
d of 12.5 ± 2.8 M at –123 mV and of 0.18 ± 0.02 mM at –62 mV The Hill coefficient (n) was close to 1 at all potentials indicating that binding of a single Ba2+ ion is sufficient to block the channel. When [K+]o was raised to 28 mM the Kd was little changed (12.4 ± 4.1 gM at –123 mV 0.27 ± 0.05 mM at –62 mV) and n was unaffected, suggesting that K+ does not interact with the Ba2+ binding site. The kinetics of Ba2+ block were slow, 10 M Ba2+ blocking the KATP current with a time constant of 20 ms at –123 mV in 28 mM [K+]o. The blocking rate constant was calculated as 1.7 mM–1 ms–1 and the unblocking rate as 0.02 ms–1, at –123 mV The data are discussed in terms of a model in which Ba2+ binds to a site at the external mouth of the channel to inhibit the KATP channel. 相似文献
19.
20.
β-Adrenergic stimulation of pacemaker cells from the sinus venosus of the cane toad (Bufo marinus) increases intracellular calcium ([Ca2+]i) and firing rate. The increase in [Ca2+]i could contribute to the increased firing rate by increasing the inward Na+-Ca2+ exchange current (I
Na-Ca) during diastole. In this study we measured [Ca2+]i and membrane currents in single, isolated, voltage-clamped pacemaker cells. We show that I
Na-Ca increases during β-adrenergic stimulation. To test whether this increase in I
Na-Ca is caused by elevated [Ca2+]i or by changes in the properties of the Na+-Ca2+ exchanger, we made rapid applications of caffeine and plotted the I
Na-Ca against [Ca2+]i. This relationship was linear during the declining phase of the [Ca2+]i signal caused by caffeine and was not significantly different in the presence or absence of β stimulation. These results
show that I
Na-Ca is increased during β-adrenergic stimulation and will contribute to the increased firing rate. However the increase in I
Na-Ca appears to be a consequence of the increase in [Ca2+]i and is not caused by changes in the intrinsic properties of the Na+-Ca2+ exchanger.
Received: 18 January 1999 / Received after revision: 9 April 1999 / Accepted: 22 April 1999 相似文献