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马齿苋多糖对 INS-1 细胞电压门控钠通道的影响。

Effects of polysaccharide from Portulaca oleracea L. on voltage-gated Na channel of INS-1 cells.

机构信息

School of Life Science, Jiangxi Science & Technology Normal University, Nanchang, Jiangxi 330013, PR China.

School of Pharmacy, Jiangxi University of Traditional Chinese Medicine, Nanchang, Jiangxi 330004, PR China.

出版信息

Biomed Pharmacother. 2018 May;101:572-578. doi: 10.1016/j.biopha.2018.02.136. Epub 2018 Mar 22.

Abstract

Our previous work showed that polysaccharide isolated from Portulaca oleracea L. (POP) has an insulinotropic effect. The voltage-gated Na channel (VGSC) in the excitement phase plays an important role. This work aims to study the effect of POP on the voltage-gated Na channel current (I) and its channel dynamic characteristics in insulin-secreting β-cell line (INS-1) cells of rat. Our results revealed that POP can inhibit the amplitude of I and improve cell survival in a concentration-dependent manner. POP concentration of 0.5 mg mL reduced the amplitude of I, suppressed the I of steady-state activation, shifted the steady-state inactivation curves of I to negative potentials, prolonged the time course of I recovery from inactivation, and enhanced the activity-dependent attenuation of I. Furthermore, 0.5 mg mL POP or low concentration of tetrodotoxin (TTX, a VGSC-specific blocker) partially inhibited I and also improved insulin synthesis and cell survival. Collectively, these results revealed that POP protects INS-1 cells and enhances the insulin synthesis in INS-1 cells, and the mechanism through the partial inhibition on I channel is strongly recommended.

摘要

我们之前的工作表明,马齿苋(Portulaca oleracea L.,POP)中分离得到的多糖具有胰岛素促分泌作用。在兴奋阶段,电压门控钠离子通道(voltage-gated Na channel,VGSC)起着重要作用。本研究旨在探讨 POP 对大鼠胰岛素分泌细胞系(INS-1)细胞的电压门控钠离子通道电流(I)及其通道动力学特性的影响。结果表明,POP 可呈浓度依赖性抑制 I 的幅度并提高细胞存活率。POP 浓度为 0.5mg/mL 时,可降低 I 的幅度,抑制 I 的稳态激活,使 I 的稳态失活曲线向负电位移动,延长 I 失活后恢复的时间过程,并增强 I 的活性依赖性衰减。此外,0.5mg/mL 的 POP 或低浓度的河豚毒素(tetrodotoxin,TTX,一种 VGSC 特异性阻断剂)部分抑制 I 并改善胰岛素的合成和细胞存活率。综上,这些结果表明,POP 可保护 INS-1 细胞并增强 INS-1 细胞中的胰岛素合成,其作用机制可能是通过对 I 通道的部分抑制。

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