Ebselen 抑制 ONOO~- 对神经元[Ca~(2+)]_i 的影响

Ｆｕｒａ－２显微荧光测钙技术研究发现,过氧亚硝基阴离子（ＯＮＯＯ－）作用于ＭＮ９Ｄ细胞,数ｓ内即可导致其胞内游离钙离子浓度（［Ｃａ２＋］ｉ）的急剧升高．胞外液换为无钙液或向胞外液中加入硝苯吡啶（Ｎｉｆｅｄｉｐ－ｉｎｅ）、二硫苏糖醇（ＤＴＴ）均可抑制ＯＮＯＯ－对［Ｃａ２＋］ｉ的影响,提示Ｌ－型钙通道的激活是ＯＮＯＯ－引起［Ｃａ２＋］ｉ升高的主要原因,ＯＮＯＯ－的这种作用可能与其氧化特性有关．Ｅｂｓｅｌｅｎ（２－苯基－１,２－苯并异硒唑－３（２Ｈ）酮）明显抑制ＯＮＯＯ－对［Ｃａ２＋］ｉ的影响,并且存在一定的剂量效应关系．     

不同浓度ET-1引起心肌细胞[Ca2+]i 升高作用的量效关系

目的：探讨内皮素－１（ＥＴ－１）对心肌细胞内游离钙浓度（［Ｃａ２＋］ｉ）的作用以及不同浓度ＥＴ－１引起［Ｃａ２＋］ｉ升高作用的量效关系。方法：采用分离的Ｓｐｒａｇｕｅ－Ｄａｗｌｅｙ大鼠心室肌细胞,以Ｆｕｒａ－２／ＡＭ荧光指示剂负载,检测不同浓度ＥＴ－１引起［Ｃａ２＋］ｉ变化。结果：ＥＴ－１引起［Ｃａ２＋］ｉ升高呈双相反应,即起始的短暂快速相和随后的持续相。在１×１０－９～５×１０７ｍｏｌ／Ｌ范围内,随着ＥＴ－１浓度的增加,其升高［Ｃａ２＋］ｉ的作用亦增强;并且这种作用可被ＥＴＡ的特异性受体阻断剂ＢＱ１２３（２×１０６ｍｏｌ／Ｌ）所阻断。结论：ＥＴ－１升高［Ｃａ２＋］ｉ呈剂量依赖关系,其作用具有特异性,并且是通过ＥＴＡ受体介导的。     

稀土La~（3＋）对α－石英细胞毒性拮抗作用的研究

本文采用家兔肺泡巨噬细胞（ＡＭ）体外培养法，以细胞存活率、细胞内游离钙离子浓度（［Ｃａ（２＋）］ｉ）为指标，研究了稀土Ｌａ（３＋）对二氧化硅细胞毒性的拮抗作用。结果提示Ｌａ（３＋）可能通过阻断细胞膜的Ｃａ（２＋）内流来达到拮抗石英细胞毒性的作用。     

低功率激光通过细胞内Ca^2＋对细胞功能的调控作用

综述了Ｈｅ－Ｎｅ激光照射使细胞溶质内［Ｃａ＾２＋］ｉ增加，产生钙信号，从而调控细胞功能，引起细胞内一系列生理和生物化学反应。     

咖啡因对大鼠肾上腺嗜铬细胞钙信号调节作用

在单个大鼠肾上腺嗜铬细胞上,采用钙显微荧光测量方法,测量了咖啡因对胞内游离钙浓度的影响。实验结果表明,在２Ｃａ６２＋外液中,咖啡因（１ｍｍｏｌ／Ｌ,１０ｍｍｏｌ／Ｌ,４０ｍｍｏｌ／Ｌ）对细胞的自发振荡表现出明显的抑制作用;对不表现自发振荡的细胞,咖啡因能引起钙浓度的升高或钙振荡,在无外钙条件下研究连续咖啡因刺激引起的钙浓度变化,发现胞内钙加易排空,但随后的含钙咖啡因刺激仍可引起钙升高。     

大鼠嗜铬细胞分泌的膜片钳和 fura-2 联合检测

在原代培养的大鼠肾上腺嗜铬细胞上,综合运用细胞内钙测定法和全细胞膜片钳法,以检测膜电容变化为手段测定单一肾上腺嗜铬细胞的胞吐过程．通过施加＋２０ｍＶ去极化时引起的钙电流,对细胞膜电容的变化以及细胞内钙浓度［Ｃａ２＋］ｉ变化的同时检测,多方位地确定影响细胞分泌的因素．     

Ebselen抑制ONOO^—对神经元[Ca^2＋]的影响

Ｆｕｒａ－２显微荧光测钙技术研究发现,过氧亚硝基阴离子作用于ＭＮ９Ｄ细胞,数ｓ内即可导致基胞内游离钙离子浓度的急剧升高。胞外液换为无钙液或向胞外液中加入硝苯吡啶 、二硫苏糖醇均可抑制ＯＮＯＯ＾－对「Ｃａ＾２＋」ｉ的影响,     

关于n~(1/2)∫_0~(π/2)(sin~nxdx(n→∞))渐近级数展开计算

运用文献［１］的结果建立了如下的渐进展开式：ｎ∫π／２０ｓｉｎｎｘｄｘ～π２∞ｉ＝０ａｉｎｉ其中，ａｌ由下面的递推公式所决定：ｌｉ＝０ａｉｂｌ－ｉ＝（－１）ｌ１／２（１／２－１）…（１／２－ｌ＋１）ｌ！，ａ０＝１，ｌ＝１，２，３式中：ｂ０＝１，ｂ１＝ａ１，ｂｉ＋１＝ａ１＋ｉ１！ａ２＋ｉ（ｉ－１）２！ａ３＋…＋ｉ（ｉ－１）…（ｉ－ｉ＋２）（ｉ－１）！ａｉ＋ｉ！ｉ！ａｉ＋１，ｉ＞１这个新递推公式的作用是简化了系数计算的复杂性。此外，还给出了有关的Ｗａｌｉｓ公式渐进性的应用。     

咖啡因对大鼠肾上腺嗜铬细胞钙信号调节作用

在单个大鼠肾上腺嗜铬细胞上，采用钙显微荧光测量方法，测量了咖啡因对胞内游离钙浓度的影响．实验结果表明，在２Ｃａ２＋外液中，咖啡因（１ｍｍｏｌ／Ｌ，１０ｍｍｏｌ／Ｌ，４０ｍｍｏｌ／Ｌ）对细胞的自发振荡表现出明显的抑制作用；对不表现自发振荡的细胞，咖啡因能引起钙浓度的升高或钙振荡．在无外钙条件下研究连续咖啡因刺激引起的钙浓度变化，发现胞内钙库易排空，但随后的含钙咖啡因刺激仍可引起钙升高．同时，在无外钙条件下施加咖啡因可检测到激素的分泌，表明由咖啡因导致的钙库释放可以独立地触发分泌     

川芎嗪对Ca^2＋促进的儿茶酚胺分泌抑制效应的研究

用胶原酶分离豚鼠肾上腺髓质嗜铬细胞，获得离体豚鼠肾上髓质嗜铬细胞悬液，可用作刺激－分泌偶联研究的模型。２．２ｍｏｌ／ＬＣａ＾２＋促进铬细胞儿茶酚胺的分泌，与无钙组比较有显著差异，不同浓度的川芎嗪与Ｃａ＾２＋的混合液作用于细胞悬液，细胞儿茶酚胺的分泌受混合液中Ｃａ＾２＋的促进，而川芎嗪无显著影响。     

Ca2+ signals induced from calcium stores in pancreatic islet β cells

In single rat pancreatic β cells,using fura-2 microfluorometry to measure [Ca2+]i response upon different stimuli,the ways of calcium regulation have been studied.When the extracellular calcium concentration was 2.5 mmol/L,either 60 mmol/L KCl,20 mmol/L D-glucose or 0.1 mmol/L tolbutamide induced increase in [Ca2+]i.Such increase in [Ca2+]i was absent when the same stimuli were applied under zero extracellular calcium.These results indicate that the increase of [Ca2+]i is induced by the activation of voltage-dependent calcium channels in β cells.The manifold forms of [Ca2+]i change induced by glucose imply that the effects of glucose are complex.5 mmol/L caffeine or 5 mmol/L MCh increase the [Ca2+]i ,which is independent of the external calcium,suggesting that [Ca2+]i can be regulated by Ca2+ release from not only the IP3-sensitive but also the ryanodine sensitive calcium stores in β cells.The latency of Ca responses for IP3 pathway (5 s) is faster than that for ryanodine pathway (30 s).It is concluded that there are multiple calcium stores in rat pancreatic β cells.     

Ca2+ signals induced from calcium stores in pancreatic islet β cells

In single rat pancreatic β cells, using fura-2 microfluorometry to measure [Ca²⁺]i response upon different stimuli, the ways of calcium regulation have been studied. When the extracellular calcium concentration was 2.5 mmol/L, either 60 mmol/L KCl, 20 mmol/L D-glucose or 0.1 mmol/L tolbutamide induced increase in [Ca²⁺]i. Such increase in [Ca²⁺]i was absent when the same stimuli were applied under zero extracellular calcium. These results indicate that the increase of [Ca²⁺]i is induced by the activation of voltage-dependent calcium channels in β cells. The manifold forms of [Ca²⁺]i change induced by glucose imply that the effects of glucose are complex. 5 mmol/L caffeine or 5 mmol/L MCh increase the [Ca²⁺]i, which is independent of the external calcium, suggesting that [Ca²⁺]i can be regulated by Ca²⁺ release from not only the IP₃-sensitive but also the ryanodine sensitive calcium stores in β cells. The latency of Ca responses for IP₃ pathway (5 s) is faster than that for ryanodine pathway (30 s). It is concluded that there are multiple calcium stores in rat pancreatic β cells.     

15 － KETE 对大鼠肺动脉平滑肌细胞钙离子浓度的影响

摘要: 目的探讨15-KETE 对大鼠肺动脉平滑肌细胞内Ca2 + 的作用及其来源。方法以酶法( 胶原酶Ⅰ型和弹性 酶) 分离培养原代大鼠肺动脉平滑肌细胞,将细胞稀释所需密度( 2 × 105 个/mL) ,加样于6 孔板中的盖玻片上,放 入37℃孵箱中培养12 h,细胞贴壁后,取出6 孔板中的盖玻片,放入特制的小槽内,D-Hanks 液冲洗细胞3 次,加入 1 × 10 － 5mol /L 的Flou-3 /AM,置37℃孵箱中避光孵育约30 min,用D-Hanks 液洗去细胞外残留染料,应用激光扫描 共聚焦显微镜技术,测定了15-KETE 对大鼠肺动脉平滑肌细胞游离钙离子浓度的影响。结果1) 15-KETE ( 1 × 10 － 8-1 × 10 － 6 ) mol /L 可依赖性引起肺动脉平滑肌细胞内钙离子浓度( ［Ca2 +］i) 增加; 2) 1 × 10 － 6 mol /L 维拉米( L-型钙离子通道阻断剂) 和无钙离子细胞外液显著阻抑了1 × 10 － 6 mol /L 15-KETE 引起肺动脉平滑肌［Ca2 +］i 增 加。结论15-KETE 可引起大鼠肺动脉平滑肌［Ca2 +］i 增加,并且此钙来源于细胞外液钙离子。     

知柏地黄丸浸液对大鼠嗜铬细胞内钙的作用

运用Fura-2显微荧光测量技术,在单个大鼠肾上腺嗜铬细胞上,测量中药知柏地黄丸浸液对胞内游离钙浓度([Ca     

Effect of Ab_(1-40) on membrane permeability and intracellular free Ca~(2+) of nerve cells

Alzheimers disease (AD) is a kind of progressive neurodegenerative disease, characterized by intracellularfibrillar tangles and extracellular senile plaques, the main component of the plaques are b-amyloid (Ab), composed of 3943 amino acids[1]. Glenner and Wong first isolated Ab peptide and determined the sequence in 1984, after-wards, a series of researches were done on its production, structure determination, aggregation, hydrophobicity, re-ceptor and cell toxicity. Ab is the abnormal fiss…     

Heterotrimeric G protein participated in modulation of cytoplasmic calcium concentration in pollen cells

Cytoplasmic free calcium concentration([Ca2+]c) in pollen cells of Lilium daviddi is measured with confocal laser scanning microscopy to investigate the effect of heterotrimeric G protein (G protein) on [Ca2+]c and the possible signal transduction pathway of G protein triggering cellular calcium signal. After application, cholera toxin (CTX), an agonist of G protein, triggers a transient increase of [Ca2+]c in pollen cells, and evokes a spatial-temporal characteristic calcium dynamics; while pertussis toxin (PTX), a G protein antagonist, leads to the decrease of [Ca2+]c. Both L-type Ca2+ channel blocker verapamil and inhibitor of IP3 receptor heparin inhibit CTX-induced [Ca2+]c increase. The results show that G protein may play a role in the modulation of [Ca2+]c through enhancing the extracellular Ca2+ influx and releasing of Ca2+ from intracellular stores.     

KCl对Hepa1-6细胞胞内钙离子浓度影响的研究

目的：分析Ka是否会引起Hepal-6细胞胞内钙离子浓度的升高,并解释相关机理。方法：KCl的浓度和负载时间可能会引起细胞内钙离子浓度的不同变化。采用比率荧光成像系统检测Hepal-6细胞的胞内钙离子浓度。结果：（1）在即时检测组中,与对照组相比,10、30、50mmol／L的Ka分别引起胞内钙离子浓度的显著升高（p〈0．05）,但各组别之间无显著差异。（2）在0．5h延迟检测组中,与对照组相比,10、30、50mmol／L的KCl分别引起胞内钙离子浓度的显著升高（p〈0．05）并且各组别之间无显著差异。此外,即时检测组与延迟检测组的结果没有显著差异。结论：10mmol／L的KCl足以引起Hepal-6细胞胞内钙离子浓度即时的显著上升。无论在即时检测组还是0．5h延迟检测组,各组别之间无显著差异。这表明当胞内的钙离子浓度上升到一定值,Ka对于胞内钙离子浓度的影响不会随其浓度的变化而发生改变。     

Ca~(2+)对水稻幼苗生长的影响

对水稻幼苗进行不同水平Ca2 + 处理 ,结果表明 :缺钙和加 0 75～ 10 5mmol/LCa2 + 处理对水稻幼苗的株高无明显影响 ;缺Ca2 + 会降低水稻幼苗的根系活力、叶绿素含量和光合强度 ;加Ca2 + 能增加水稻幼苗根冠比和根系活力 ;加低浓度 ( 0 75～ 1 5mmol/L)Ca2 + 可增加水稻幼苗的干物重、叶绿素含量和光合强度 ,促进水稻幼苗生长 ;加高浓度 ( 5 5～ 10 5mmol/L)Ca2 + 则降低叶绿素含量和光合强度 ,对水稻幼苗生长产生抑制作用