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钩藤羧烷基酯可增强噪声损伤后感觉神经功能的恢复。

Carboxy alkyl esters of Uncaria tomentosa augment recovery of sensorineural functions following noise injury.

机构信息

Research Service-151, Loma Linda Veterans Affairs Hospital, Loma Linda, CA 92357, USA. O'

出版信息

Brain Res. 2011 Aug 17;1407:97-106. doi: 10.1016/j.brainres.2011.06.044. Epub 2011 Jun 24.

Abstract

This study tested the hypothesis that hydrophilic chemotypes of the medicinal vine Uncaria tomentosa (UT) would facilitate recovery of sensorineural functions following exposure to a damaging level of noise. The particular chemotypes investigated were carboxy alkyl esters (CAE) which are known to exhibit multifunctional cytoprotective properties that include: enhanced cellular DNA repair, antioxidation and anti-inflammation. Long-Evans rats were divided into four treatment groups: vehicle-control, noise-only, CAE-only and CAE+noise. The noise exposure was an 8kHz octave band of noise at 105dB SPL for 4h. Outer hair cell (OHC) function was measured with the cubic 2f(1)-f(2) distortion product otoacoustic emissions (DPOAE) at the start of the study (baseline) and at time-points that corresponded to 1day, 1week and 4weeks post-noise exposure to determine within-group effects. Compound action potentials to puretone stimuli were recorded from the VIIIth craniofacial nerve at 4weeks post-noise exposure to determine between-group effects. Additionally, cytocochleograms were constructed for each row of OHCs from each group. Noise exposure produced significant sensorineural impairments. However, CAE treatment facilitated almost complete recovery of OHC function and limited the magnitude of cell loss. The loss of neural sensitivity to puretone stimuli was inhibited with CAE treatment. Therefore, it appears that the multifunctional cytoprotective capacity of CAE from UT may generalize to otoprotection from acoustic over-exposure.

摘要

本研究检验了这样一个假设,即药用钩藤(UT)的亲水性化学型将促进感觉神经功能在暴露于破坏性噪声水平后的恢复。研究中调查的特定化学型是羧基烷基酯(CAE),其已知具有多种细胞保护特性,包括:增强细胞 DNA 修复、抗氧化和抗炎。长耳大鼠被分为四个治疗组:载体对照组、噪声组、CAE 组和 CAE+噪声组。噪声暴露是 105dB SPL 的 8kHz 倍频程噪声,持续 4 小时。在研究开始时(基线)和噪声暴露后 1 天、1 周和 4 周的时间点测量外毛细胞(OHC)功能,使用立方 2f(1)-f(2) 失真产物耳声发射(DPOAE),以确定组内效应。在噪声暴露后 4 周记录来自 VIII 颅面神经的纯音刺激复合动作电位,以确定组间效应。此外,为每组的每一排 OHC 构建细胞 Cochleogram。噪声暴露导致明显的感觉神经损伤。然而,CAE 治疗促进了 OHC 功能的几乎完全恢复,并限制了细胞损失的程度。CAE 治疗抑制了对纯音刺激的神经敏感性损失。因此,似乎来自 UT 的 CAE 的多功能细胞保护能力可推广到对声过度暴露的耳保护。

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