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麦冬皂苷单体DT-13可降低成年大鼠心室肌细胞缺氧时的L型钙电流。

The saponin monomer of dwarf lilyturf tuber, DT-13, reduces L-type calcium currents during hypoxia in adult rat ventricular myocytes.

作者信息

Tao Jin, Wang Hongyi, Zhou Hong, Li Shengnan

机构信息

Department of Pharmacology, Nanjing Medical University, Hanzhong Road 140, Nanjing 210029, PR China.

出版信息

Life Sci. 2005 Oct 28;77(24):3021-30. doi: 10.1016/j.lfs.2005.01.039. Epub 2005 Jun 23.

Abstract

The saponin monomer 13 of dwarf lilyturf tuber (DT-13), one of the saponin monomers of dwarf lilyturf tuber, has been found to have potent cardioprotective effects. In order to investigate the effects of DT-13 on L-type calcium currents (I(Ca,L)), exploring the mechanisms of DT-13's cardioprotective effects in the condition of pathophysiology, we directly measured the I(Ca,L) during hypoxia in the adult rat cardiac myocytes exposed to DT-13 using standard whole-cell patch-clamp recording technique. Our previous results showed that DT-13 exerted decreasing effects on the I(Ca,L) of the single adult rat cardiac myocytes. In the condition of hypoxia, the current density was inhibited by about 29% after exposure of the cells to DT-13 (0.1 micromol L(-1)) for 10 min, from 6.96+/-1.05 pA/pF to 4.38+/-0.35 pA/pF (n=5, P<0.05). This I(Ca,L)-inhibiting action of DT-13 was concentration-dependent and showed no frequency-dependence. DT-13 up-shifted the current-voltage (I-V) curve. Steady-state activation of I(Ca,L) was not affected markedly, and the half activation potential (V(0.5)) in the presence of DT-13 (0.1 micromol L(-1)) was also not significantly different. DT-13 at 0.1 micromol L(-1) markedly accelerated the voltage-dependent steady-state inactivation of calcium current and shifted the steady-state inactivation curve of I(Ca,L) to the left. In combination with previous reports, these results suggest that there might be a close relationship between the cardioprotective effects of DT-13 and L-type calcium channels in the condition of hypoxia.

摘要

麦冬皂苷单体13(DT - 13)是麦冬的皂苷单体之一,已被发现具有强大的心脏保护作用。为了研究DT - 13对L型钙电流(I(Ca,L))的影响,探索DT - 13在病理生理条件下心脏保护作用的机制,我们采用标准的全细胞膜片钳记录技术,直接测量了成年大鼠心肌细胞在缺氧状态下暴露于DT - 13时的I(Ca,L)。我们之前的结果表明,DT - 13对单个成年大鼠心肌细胞的I(Ca,L)有降低作用。在缺氧条件下,细胞暴露于DT - 13(0.1 μmol L(-1))10分钟后,电流密度从6.96±1.05 pA/pF抑制至4.38±0.35 pA/pF(n = 5,P<0.05),约抑制了29%。DT - 13的这种I(Ca,L)抑制作用呈浓度依赖性,且无频率依赖性。DT - 13使电流 - 电压(I - V)曲线向上移位。I(Ca,L)的稳态激活没有明显受到影响,在存在DT - 13(0.1 μmol L(-1))时的半激活电位(V(0.5))也没有显著差异。0.1 μmol L(-1)的DT - 13显著加速了钙电流的电压依赖性稳态失活,并使I(Ca,L)的稳态失活曲线向左移位。结合之前的报道,这些结果表明在缺氧条件下,DT - 13的心脏保护作用与L型钙通道之间可能存在密切关系。

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