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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >LPA-mediated demyelination in ex vivo culture of dorsal root.
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LPA-mediated demyelination in ex vivo culture of dorsal root.

机译：LPA介导的背根离体培养中的脱髓鞘作用。

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摘要

Lysophosphatidic acid (LPA) causes neuropathic pain with demyelination in sensory fibers. In dorsal root (DR) ex vivo culture, the addition of 0.1 microM LPA caused a characteristic demyelination at 24h in scanning and transmission electron microscopy analyses. Moreover, direct contact between C-fibers due to loss of partition by Schwann cell in Remak bundles was observed. LPA-induced demyelination of DR was concentration-dependent in the range between 0.01 and 1M, and was abolished by BoNT/C3 and Y-27632, a RhoA and Rho kinase inhibitor, respectively. The demyelination was equivalent between the preparations with and without dorsal root ganglion. LPA also caused a down-regulation of myelin proteins, such as myelin basic protein (MBP) and myelin protein zero (MPZ) to approximately 70% of control. All these findings suggest that the demyelination observed in the neuropathic pain due to nerve injury occurs through a direct action of LPA on Schwann cells.
机译：溶血磷脂酸（LPA）引起神经性疼痛，感觉纤维脱髓鞘。在离体背根（DR）的体外培养中，在扫描和透射电子显微镜分析中，添加0.1 microM LPA会在24小时引起特征性脱髓鞘。此外，观察到由于Remak束中Schwann细胞失去分配作用，导致C纤维之间直接接触。 LPA诱导的DR脱髓鞘在0.01到1M之间是浓度依赖性的，并且分别被RhoA和Rho激酶抑制剂BoNT / C3和Y-27632废除。具有和不具有背根神经节的制剂之间的脱髓鞘作用相等。 LPA还导致髓磷脂蛋白（例如髓磷脂碱性蛋白（MBP）和髓磷脂零蛋白（MPZ））下调至对照的约70％。所有这些发现表明，在神经损伤引起的神经性疼痛中观察到的脱髓鞘是通过LPA对雪旺氏细胞的直接作用而发生的。

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