以下文章来源于食品放大镜 ，作者文献解读
四川大学华西医院魏欣团队发表鱼油用于治疗青光眼封面综述
近日，四川大学华西医院Huali Ye、Yunyi Liu(共同第一作者)、魏欣教授(通讯作者)和乐山市人民医院Zhike Xu在国际期刊《Molecule Nutrition and Food Research》(Q1，IF：6.575)发表了题为“Fish Oil in Glaucoma Treatment: From Biological Functions to Clinical Potential”的封面综述。
青光眼是世界范围内引起视力下降的主要原因，多种风险因素影响其发病机制和进程，包括年龄、增加的眼内压 (IOP)、低级别炎症、氧化应激、眼血流不足等。目前，降IOP疗法是控制青光眼进程最有效方法。然而，由于不足反应和持续视网膜神经变性，结果往往不令人满意。近年来，一些研究报道鱼油(一种ω-3膳食补充剂)有益于青光眼患者，然而其功效和潜在机制仍然不清楚。有趣的是，青光眼患者具有更低的ω-3脂肪酸血液水平，特别是DHA和EPA。患者饮食补充ω-3可能使脂肪酸水平正常，从而提升其作用。所以，鱼油可能是青光眼治疗研究一个新的关注领域。在该综述中，作者总结了鱼油中的活性成分在延缓青光眼发展中的作用，包括降低IOP、调节血液供应、缓解炎症和减少氧化应激。
鱼油是ω-3脂肪酸的一个合适膳食来源，它主要含有DHA和EPA。相关研究主要关注ω-3脂肪酸，其在视网膜氧化应激、IOP管理、血液供应、炎症中发挥关键作用，从而有助于减少与青光眼相关的潜在损伤。膳食补充鱼油可能对青光眼患者的治疗和预知产生积极作用。然而，鱼油的神经保护作用仍需要被证实，需要更多的研究来探究其中机制。另外，迫切需要更多的试验来证实临床中的功效。对鱼油未来的研究可能关注以下方面：1）加深对鱼油在视网膜中代谢的理解；2）证实ω-3脂肪酸在青光眼发展中的生物学功能和临床功效；3）探究鱼油补充的量效关系；4）进行更多的临床试验来证实鱼油在青光眼中的功效。
Table 1. The roles of active ingredients in fish oil in delaying glaucoma development.
Fig.1 The potential mechanism by which omega-3 fatty acids lower IOP. In glaucoma, the aqueous humor outflow pathway is blocked, leading to high IOP and nerve damage. I: Omega-3 fatty acids suppress the development of cross-linked actin networks, which improves the aqueous outflow and reduces IOP. II: The metabolites of omega-3 fatty acids reduced inflammation in the trabecular and uveoscleral outflow pathways and subsequently promoted aqueous outflow. III: Omega-3 fatty acids influence the concentration of endogenous prostaglandin F to lower IOP.
Fig.2 The potential mechanism by which omega-3 fatty acids affects blood flow and red blood cells. I: Omega-3 fatty acids reduce blood viscosity and modulate optic nerve blood flow. II: EPA inhibits platelet aggregation and dilates blood vessels to irregular blood flow. III: Omega-3 fatty acids affect the membrane composition of RBCs. DHA, docosahexaenoic acid; EPA, eicosapentaenoic acid; PL, phospholipid; RBCs, red blood cells.
Fig.3 The potential mechanism by which omega-3 fatty acids alleviate inflammation. Microglia can polarize into M1 proinflammatory and M2 anti-inflammatory phenotypes. Omega-3 fatty acids can promote the shift of microglia from M1 to M2. Omega-3 fatty acids can antagonize the NF-κB pathway, which can facilitate the shift from M1 to M2 and decrease proinflammatory factors. Omega-3 fatty acids can promote the function of M2 macrophages to inhibit apoptosis and improve neurological functions. IL, interleukin; iNOS, inducible nitric oxide synthase; M1, macrophage M1; M2, macrophage M2; TNF-α, tumor necrosis factor-alpha.
Fig.4 The potential mechanism by which omega-3 fatty acids diminish oxidative stress. I: Omega-3 fatty acids have H2O2-mediated anti-proliferative/-metabolic antioxidant effects. II: Retinal neurons could elongate and desaturate EPA to synthesize DHA for neuroprotection. III: EPA rescues photoreceptors from apoptosis induced by hydrogen peroxide through the ERK/MAPK signaling pathway. IV: DHA promotes NPD1 production and inhibits oxidative stress, thereby promoting the survival of RPEs and PRCs. DHA, docosahexaenoic acid; EPA, eicosapentaenoic acid; Hsp90, heat shock protein 90; NPD1, neuroprotectin D1; PL, phospholipid; PRCs, photoreceptor cells; RPEs, retinal pigment epithelium cells.
原文链接
https://doi.org/10.1002/mnfr.202200727
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