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丁香酚引起的皂苷去皮纤维收缩受到肝素或兰尼碱受体阻滞剂的抑制。

Eugenol-induced contractions of saponin-skinned fibers are inhibited by heparin or by a ryanodine receptor blocker.

作者信息

Lofrano-Alves Marco S, Oliveira Edson L, Damiani Carlos E N, Kassouf-Silva Ilana, Fogaça Rosalvo T H

机构信息

Departamento de Fisiologia, Setor de Ciências Biológicas, Centro Politécnico, Universidade Federal do Paraná, Curitiba, Paraná, Brazil.

出版信息

Can J Physiol Pharmacol. 2005 Dec;83(12):1093-100. doi: 10.1139/y05-104.

Abstract

The effects of eugenol on the sarcoplasmic reticulum (SR) and contractile apparatus of chemically skinned skeletal muscle fibers of the frog Rana catesbeiana were investigated. In saponin-skinned fibers, eugenol (5 mmol/L) induced muscle contractions, probably by releasing Ca(2+) from the SR. The Ca(2+)-induced Ca(2+) release blocker ruthenium red (10 micromol/L) inhibited both caffeine- and eugenol-induced muscle contractions. Ryanodine (200 micromol/L), a specific ryanodine receptor/Ca(2+) release channel blocker, promoted complete inhibition of the contractions induced by caffeine, but only partially blocked the contractions induced by eugenol. Heparin (2.5 mg/mL), an inositol 1,4,5-trisphosphate (InsP3) receptor blocker, strongly inhibited the contractions induced by eugenol but had only a small effect on the caffeine-induced contractions. Eugenol neither altered the Ca(2+) sensitivity nor the maximal force in Triton X-100 skinned muscle fibers. These data suggest that muscle contraction induced by eugenol involves at least 2 mechanisms of Ca(2+) release from the SR: one related to the activation of the ryanodine receptors and another through a heparin-sensitive pathway.

摘要

研究了丁香酚对牛蛙(Rana catesbeiana)化学去皮肤骨骼肌纤维的肌浆网(SR)和收缩装置的影响。在皂素去皮肤纤维中,丁香酚(5 mmol/L)可能通过从SR释放Ca(2+)诱导肌肉收缩。Ca(2+)诱导的Ca(2+)释放阻滞剂钌红(10 μmol/L)抑制咖啡因和丁香酚诱导的肌肉收缩。Ryanodine(200 μmol/L),一种特异性ryanodine受体/Ca(2+)释放通道阻滞剂,促进完全抑制咖啡因诱导的收缩,但仅部分阻断丁香酚诱导的收缩。肝素(2.5 mg/mL),一种肌醇1,4,5-三磷酸(InsP3)受体阻滞剂,强烈抑制丁香酚诱导的收缩,但对咖啡因诱导的收缩只有很小的影响。丁香酚既不改变Triton X-100去皮肤肌纤维中的Ca(2+)敏感性,也不改变最大力量。这些数据表明,丁香酚诱导的肌肉收缩至少涉及SR释放Ca(2+)的两种机制:一种与ryanodine受体的激活有关,另一种通过肝素敏感途径。

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