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在大鼠视网膜中评估的两种神经保护剂——膳食藏红花和光生物调节作用的时间进程。

The time course of action of two neuroprotectants, dietary saffron and photobiomodulation, assessed in the rat retina.

作者信息

Marco Fabiana Di, Romeo Stefania, Nandasena Charith, Purushothuman Sivaraman, Adams Charean, Bisti Silvia, Stone Jonathan

机构信息

Department of Biotechnology and Applied Clinical Science, University of L'Aquila Italy.

出版信息

Am J Neurodegener Dis. 2013 Sep 18;2(3):208-20. eCollection 2013.

PMID:24093084
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3783833/
Abstract

BACKGROUND

Dietary saffron and photobiomodulation (low-level infrared radiation, PBM) are emerging as therapeutically promising protectants for neurodegenerative conditions, such as the retinal dystrophies. In animal models, saffron and PBM, given in limited daily doses, protect retina and brain from toxin- or light-induced stress. This study addresses the rate at which saffron and PBM, given in daily doses, induce neuroprotection, using a light damage model of photoreceptor degeneration in Sprague Dawley (SD) rats.

RESULTS

Rats were raised in dim cyclic (12 h 5 lux, 12 h dark) illumination, treated with saffron or PBM for 2-10 d, and then exposed to bright damaging light (1,000 lux for 24 h). After 1 week survival, the retina was assessed for photoreceptor death (using the TUNEL reaction), for surviving photoreceptor damage (thickness of the outer nuclear layer) and for the expression of a stress-related protein GFAP, using immunohistochemistry. Preconditioning the retina with saffron or PBM reduced photoreceptor death, preserved the population of surviving photoreceptors and reduced the upregulation of GFAP in Müller cells. At the daily dose of saffron used (1 mg/kg), protection was detectable at 2 d, increasing to 10 d. At the daily dose of PBM used (5 J/cm(2) at 670 nm) protection was detectable at 5 d, increasing to 7-10 d.

CONCLUSIONS

The results provide time parameters for exploration of the mechanisms and durability of the protection provided by saffron and PBM.

摘要

背景

饮食中的藏红花和光生物调节(低水平红外辐射,PBM)正成为神经退行性疾病(如视网膜营养不良)具有治疗前景的保护剂。在动物模型中,每天给予有限剂量的藏红花和PBM可保护视网膜和大脑免受毒素或光诱导的应激。本研究使用Sprague Dawley(SD)大鼠光感受器变性的光损伤模型,探讨每天给予藏红花和PBM诱导神经保护的速率。

结果

大鼠在昏暗的循环光照(12小时5勒克斯,12小时黑暗)下饲养,用藏红花或PBM处理2 - 10天,然后暴露于明亮的损伤光(1000勒克斯,持续24小时)。存活1周后,通过免疫组织化学评估视网膜的光感受器死亡情况(使用TUNEL反应)、存活光感受器的损伤情况(外核层厚度)以及应激相关蛋白GFAP的表达。用藏红花或PBM预处理视网膜可减少光感受器死亡,保留存活光感受器的数量,并减少Müller细胞中GFAP的上调。在所使用的藏红花每日剂量(1毫克/千克)下,2天时可检测到保护作用,至10天时增强。在所使用的PBM每日剂量(670纳米波长下5焦耳/平方厘米)下,5天时可检测到保护作用,至7 - 10天时增强。

结论

这些结果为探索藏红花和PBM提供的保护机制及持久性提供了时间参数。

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