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泛醌,一种脂溶性抗氧化剂,对神经元电压门控钠离子电流的调制作用。

The Modulation of Ubiquinone, a Lipid Antioxidant, on Neuronal Voltage-Gated Sodium Current.

机构信息

Department of Pediatrics, Chi-Mei Medical Center, Tainan 71004, Taiwan.

Department of Physiology, National Cheng Kung University Medical College, Tainan 70101, Taiwan.

出版信息

Nutrients. 2022 Aug 18;14(16):3393. doi: 10.3390/nu14163393.

DOI:10.3390/nu14163393
PMID:36014898
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9413396/
Abstract

Ubiquinone, composed of a 1,4-benzoquinone and naturally produced in the body, actively participates in the mitochondrial redox reaction and functions as an endogenous lipid antioxidant, protecting against peroxidation in the pituitary-dependent hormonal system. However, the questions of if and how ubiquinone directly affects neuronal ionic currents remain largely unsettled. We investigated its effects on ionic currents in pituitary neurons (GH3 and MMQ cells) with the aid of patch-clamp technology. Ubiquinone decreased the peak amplitude of the voltage-gated Na current () with a slowing of the inactivation rate. Neither menadione nor superoxide dismutase modified the ubiquinone-induced inhibition. In response to an isosceles-triangular ramp pulse, the persistent () at high- and low- threshold potentials occurred concurrently with a figure-eight hysteresis loop. With ubiquinone, the increased with no change in the intersection voltage, and the magnitude of the voltage-dependent hysteresis of the current was enhanced. Ubiquinone was ineffective in modifying the gating of hyperpolarization-activated cation currents. In MMQ lactotrophs, ubiquinone effectively decreased the amplitude of the and the current inactivation rate. In sum, the effects of ubiquinone demonstrated herein occur upstream of its effects on mitochondrial redox processes, involved in its modulation of sodium channels and neuronal excitability.

摘要

泛醌由 1,4-苯醌组成,在体内自然产生,它积极参与线粒体氧化还原反应,作为内源性脂类抗氧化剂,防止垂体依赖性激素系统中的过氧化。然而,泛醌是否以及如何直接影响神经元离子电流的问题仍未得到解决。我们利用膜片钳技术研究了它对垂体神经元(GH3 和 MMQ 细胞)离子电流的影响。泛醌降低了电压门控 Na 电流()的峰值幅度,同时使失活速率减慢。甲萘醌和超氧化物歧化酶都不能改变泛醌诱导的抑制作用。在等腰三角形斜坡脉冲的刺激下,在高和低阈值电位下同时出现持续的(),并出现八角形滞后环。在泛醌存在的情况下,随着交点电压不变,电流的电压依赖性滞后幅度增加,而持续时间增加。泛醌不能改变超极化激活阳离子电流的门控。在 MMQ 催乳细胞中,泛醌有效地降低了电流的幅度和失活速率。总之,本文中观察到的泛醌的作用发生在其对线粒体氧化还原过程的作用之前,涉及到对钠通道和神经元兴奋性的调节。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bffc/9413396/0f1d7cb30066/nutrients-14-03393-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bffc/9413396/107ee35572ca/nutrients-14-03393-g001a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bffc/9413396/f2f9c9855ce2/nutrients-14-03393-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bffc/9413396/6359e1a649a5/nutrients-14-03393-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bffc/9413396/da260b2cb1ac/nutrients-14-03393-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bffc/9413396/07ba772a3a01/nutrients-14-03393-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bffc/9413396/0f1d7cb30066/nutrients-14-03393-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bffc/9413396/107ee35572ca/nutrients-14-03393-g001a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bffc/9413396/f2f9c9855ce2/nutrients-14-03393-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bffc/9413396/6359e1a649a5/nutrients-14-03393-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bffc/9413396/da260b2cb1ac/nutrients-14-03393-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bffc/9413396/07ba772a3a01/nutrients-14-03393-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bffc/9413396/0f1d7cb30066/nutrients-14-03393-g006.jpg

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