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细胞内钙离子释放机制的抑制剂可阻止毒蕈碱诱导的大鼠舌下黏液腺泡中的钙离子内流。

Inhibitors of the intracellular Ca2+ release mechanism prevent muscarinic-induced Ca2+ influx in rat sublingual mucous acini.

作者信息

Zhang G H, Melvin J E

机构信息

Department of Dental Research, University of Rochester, NY 14642.

出版信息

FEBS Lett. 1993 Jul 19;327(1):1-6. doi: 10.1016/0014-5793(93)81026-v.

Abstract

The effects of inhibitors of the intracellular Ca2+ release mechanism on divalent cation fluxes were examined in acinar cells loaded with the Ca(2+)-sensitive, Mn(2+)-quenchable dye, fura-2. TMB-8 and dantrolene (DTL) dramatically inhibited the carbachol (CCh)-stimulated increase in [Ca2+]i and Mn2+ influx. These agents do not directly inhibit divalent cation entry since addition of TMB-8 or DTL after CCh stimulation did not block Mn2+ influx. TMB-8 did not influence the [Ca2+]i increase or the Mn2+ influx produced by thapsigargin. These results indicate that TMB-8 and DTL do not interfere with divalent cation influx by inhibiting a step distal to depletion of the intracellular Ca2+ pool. TMB-8 and DTL did not significantly influence the muscarinic-stimulated production of inositol trisphosphate (IP3) and inositol tetrakisphosphate (IP4), although TMB-8, but not DTL, did decrease the CCh-stimulated 1,4,5-IP3 levels approximately 55%. The above results directly demonstrate that the filling state of the intracellular Ca2+ store primarily regulates the Ca2+ entry mechanism in sublingual mucous acinar cells.

摘要

在加载了对Ca(2+)敏感、可被Mn(2+)淬灭的染料fura-2的腺泡细胞中,研究了细胞内Ca2+释放机制抑制剂对二价阳离子通量的影响。TMB-8和丹曲林(DTL)显著抑制了卡巴胆碱(CCh)刺激引起的[Ca2+]i升高和Mn2+内流。这些药物并不直接抑制二价阳离子的进入,因为在CCh刺激后添加TMB-8或DTL并没有阻断Mn2+内流。TMB-8不影响毒胡萝卜素引起的[Ca2+]i升高或Mn2+内流。这些结果表明,TMB-8和DTL不会通过抑制细胞内Ca2+池耗竭远端的步骤来干扰二价阳离子内流。TMB-8和DTL对毒蕈碱刺激产生的肌醇三磷酸(IP3)和肌醇四磷酸(IP4)没有显著影响,尽管TMB-8(而非DTL)确实使CCh刺激的1,4,5-IP3水平降低了约55%。上述结果直接表明,细胞内Ca2+储存的充盈状态主要调节舌下粘液腺泡细胞中的Ca2+进入机制。

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