Ophthalmology Unit, Department of Head/Neck Pathologies, Policlinico San Martino Hospital, IRCCS Hospital-University San Martino, Viale Benedetto XV, 16132 Genoa, Italy.
Eye Clinic, Department of Neuroscience and Sensory Organs, University of Genoa, Policlinico San Martino Hospital IRCCS Hospital-University San Martino, Viale Benedetto XV, 16132 Genoa, Italy.
Nutrients. 2019 Jan 22;11(2):239. doi: 10.3390/nu11020239.
Glaucoma is a multifactorial disease in which pro-apoptotic signals are directed to retinal ganglion cells. During this disease the conventional outflow pathway becomes malfunctioning. Aqueous humour builds up in the anterior chamber, leading to increased intraocular pressure. Both of these events are related to functional impairment. The knowledge of molecular mechanisms allows us to better understand the usefulness of substances that can support anti-glaucoma therapy. The goal of glaucoma therapy is not simply to lower intraocular pressure; it should also be to facilitate the survival of retinal ganglion cells, as these constitute the real target tissue in this disease, in which the visual pathway is progressively compromised. Indeed, an endothelial dysfunction syndrome affecting the endothelial cells of the trabecular meshwork occurs in both normal-tension glaucoma and high-tension glaucoma. Some substances, such as polyunsaturated fatty acids, can counteract the damage due to the molecular mechanisms - whether ischemic, oxidative, inflammatory or other - that underlie the pathogenesis of glaucoma. In this review, we consider some molecules, such as polyphenols, that can contribute, not only theoretically, to neuroprotection but which are also able to counteract the metabolic pathways that lead to glaucomatous damage. Ginkgo biloba extract, for instance, improves the blood supply to peripheral districts, including the optic nerve and retina and exerts a neuro-protective action by inhibiting apoptosis. Polyunsaturated fatty acids can protect the endothelium and polyphenols exert an anti-inflammatory action through the down-regulation of cytokines such as TNF-α and IL-6. All these substances can aid anti-glaucoma therapy by providing metabolic support for the cells involved in glaucomatous injury. Indeed, it is known that the food we eat is able to change our gene expression.
青光眼是一种多因素疾病,其中凋亡信号被导向视网膜神经节细胞。在这种疾病中,传统的流出途径会出现故障。房水在前房积聚,导致眼内压升高。这两种情况都与功能障碍有关。对分子机制的了解使我们能够更好地理解可以支持抗青光眼治疗的物质的用途。青光眼治疗的目的不仅是降低眼内压,还应该促进视网膜神经节细胞的存活,因为这些细胞是这种疾病中真正的靶组织,在这种疾病中,视觉通路逐渐受损。事实上,正常眼压性青光眼和高眼压性青光眼都会发生影响小梁网内皮细胞的内皮功能障碍综合征。一些物质,如多不饱和脂肪酸,可以对抗分子机制引起的损伤,这些分子机制包括缺血、氧化、炎症或其他,这些损伤是青光眼发病机制的基础。在这篇综述中,我们考虑了一些分子,如多酚,它们不仅可以在理论上,而且还可以对抗导致青光眼损伤的代谢途径,从而有助于神经保护。例如,银杏叶提取物可以改善包括视神经和视网膜在内的外周区域的血液供应,并通过抑制细胞凋亡发挥神经保护作用。多不饱和脂肪酸可以保护内皮细胞,多酚通过下调 TNF-α和 IL-6 等细胞因子发挥抗炎作用。所有这些物质都可以通过为参与青光眼损伤的细胞提供代谢支持来辅助抗青光眼治疗。事实上,我们知道我们吃的食物能够改变我们的基因表达。