论文部分内容阅读
应用ＡＲＣＭＭＩＣ阳离子测定系统，研究ＴＭＢ８对体外新生ＳＤ大鼠单个脑细胞内游离钙的抑制作用及其机制。结果表明，在无细胞外钙情况下，静息［Ｃａ２＋］ｉ为７９±１３ｎｍｏｌ·Ｌ－１。ＴＭＢ８１０，３０μｍｏｌ·Ｌ－１能明显降低静息［Ｃａ２＋］ｉ。ＴＭＢ８１００μｍｏｌ·Ｌ－１对高钾去极化引起的［Ｃａ２＋］ｉ显著增高无明显影响。在细胞外钙为１３ｍｍｏｌ·Ｌ－１时，去甲肾上腺素诱导的细胞内［Ｃａ２＋］ｉ升高可部分被ＴＭＢ８抑制；ＴＭＢ８（３０μｍｏｌ·Ｌ－１）对ＢＨＱ引起的［Ｃａ２＋］ｉ的升高无明显抑制作用。而当细胞外液［Ｃａ２＋］ｉ为０时，ＴＭＢ８几乎完全抑制了去甲肾上腺素和ＢＨＱ的作用。提示ＴＭＢ８降低脑细胞内游离钙的作用机制是通过促使细胞内钙进入肌浆网以抑制内钙的释放，并通过饱和肌浆网内Ｃａ２＋间接地阻滞细胞膜钙通道。
Application of AR CM MIC cationic assay system to study the TMB 8 of neonatal SD rat single brain intracellular free calcium inhibition and its mechanism. The results showed that resting [Ca2 +] i was 79 ± 13 nmol·L-1 in the absence of extracellular calcium. TMB 810, 30μmol·L-1 can significantly reduce resting [Ca2] i. TMB 800μmol·L-1 high potassium depolarization caused by [Ca2] i significantly increased no significant effect. In the extracellular calcium 1 3mmol · L-1, norepinephrine-induced intracellular [Ca2 +] i increased partly by TMB 8 inhibition; TMB 8 (30μmol·L-1) caused by BHQ No significant inhibition of [Ca2 +] i increase. When extracellular Ca2 + i was 0, TMB-8 almost completely inhibited the effect of norepinephrine and BHQ. Tip TMB 8 to reduce intracellular free calcium mechanism of action is through the intracellular calcium into the sarcoplasmic reticulum to inhibit the release of calcium and saturating the sarcoplasmic reticulum Ca2 + indirectly block the cell membrane calcium channel.