首页> 美国卫生研究院文献>Nutrients >A Dietary Combination of Forskolin with Homotaurine Spearmint and B Vitamins Protects Injured Retinal Ganglion Cells in a Rodent Model of Hypertensive Glaucoma
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A Dietary Combination of Forskolin with Homotaurine Spearmint and B Vitamins Protects Injured Retinal Ganglion Cells in a Rodent Model of Hypertensive Glaucoma

机译:弗斯高林与高牛磺酸留兰香和B类维生素的饮食组合在高血压青光眼啮齿动物模型中保护受损的视网膜神经节细胞

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摘要

There is indication that nutritional supplements protect retinal cells from degeneration. In a previous study, we demonstrated that dietary supplementation with an association of forskolin, homotaurine, spearmint extract and B vitamins efficiently counteracts retinal dysfunction associated with retinal ganglion cell (RGC) death caused by optic nerve crush. We extended our investigation on the efficacy of dietary supplementation with the use of a mouse model in which RGC degeneration depends as closely as possible on intraocular pressure (IOP) elevation. In this model, injecting the anterior chamber of the eye with methylcellulose (MCE) causes IOP elevation leading to RGC dysfunction. The MCE model was characterized in terms of IOP elevation, retinal dysfunction as determined by electrophysiological recordings, RGC loss as determined by brain-specific homeobox/POU domain protein 3A immunoreactivity and dysregulated levels of inflammatory and apoptotic markers. Except for IOP elevation, dysfunctional retinal parameters were all recovered by dietary supplementation indicating the involvement of non-IOP-related neuroprotective mechanisms of action. Our hypothesis is that the diet supplement may be used to counteract the inflammatory processes triggered by glial cell activation, thus leading to spared RGC loss and the preservation of visual dysfunction. In this respect, the present compound may be viewed as a potential remedy to be added to the currently approved drug therapies for improving RGC protection.
机译:有迹象表明营养补品可保护视网膜细胞免于变性。在先前的研究中,我们证明饮食补充福斯高林,高牛磺酸,留兰香提取物和B族维生素可以有效地抵消与视神经挤压引起的视网膜神经节细胞(RGC)死亡相关的视网膜功能障碍。我们使用RGC变性尽可能取决于眼内压(IOP)升高的小鼠模型扩展了对膳食补充功效的研究。在该模型中,向眼前房注射甲基纤维素(MCE)会导致IOP升高,从而导致RGC功能障碍。 MCE模型的特征在于眼压升高,通过电生理记录确定的视网膜功能障碍,通过脑特异性同源盒/ POU域蛋白3A免疫反应性确定的RGC丢失以及炎症和凋亡标记物的水平失调。除眼压升高外,所有功能失调的视网膜参数均通过饮食补充得以恢复,表明参与了非IOP相关的神经保护作用机制。我们的假设是,膳食补充剂可用于抵消由胶质细胞激活触发的炎症过程,从而导致多余的RGC丢失和视觉功能障碍的保留。在这方面,本发明化合物可以被视为添加到当前批准的药物疗法中以改善RGC保护的潜在疗法。

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