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白内障的药物治疗及研究进展

Pharmacological treatment and research progress of cataracts

来源期刊： 眼科学报 | 2025年7月 第40卷 第7期： 565-573 发布时间：2025-07-28 收稿时间：2025/7/23 14:59:45 阅读量：16
作者：
卫佳奇,
张琇雯,
黄滔敏,
关键词：
白内障发病机制治疗药物药物研发新靶点
cataract pathogenesis therapeutic drugs drug development new targets
DOI：
10.12419/25041507
收稿时间：
2025-04-21 
修订日期：
2025-05-26 
接收日期：
2025-06-04 
白内障是全球第一大致盲眼病，表现为由多种原因导致的晶状体病变，进而出现视物模糊的现象，严重者会进一步丧失视力。白内障的类型较多，发病机制尚未完全阐释清楚，氧化应激是目前公认的主要影响因素。药物治疗一直是白内障患者临床治疗的一大难题，目前市面上还没有能够真正逆转白内障的药物，现有的药物仅能在一定程度上缓解白内障的进展。手术治疗仍是现阶段唯一有效的治疗方式，但经济因素和术后并发症的风险限制了部分患者通过手术恢复视力。白内障的治疗一直是眼科领域研究的重点，目前研究主要集中在两个战略方向上：优化手术技术并结合更优的围术期药物治疗方案以减少并发症，以及对疾病机制进行基础研究以促进新靶点药物的发现。有效的药物治疗一直是目前临床治疗的一大缺口，近年来研究者在白内障机制探索和新药研发上取得了显著进展，多个新的治疗靶点以及相关治疗药物不断被发现，但相关药物真正进入临床还面临着诸多挑战。文章主要从机制研究进展、药物治疗现状和前景较好的白内障药物临床研究进展等进行综述，旨在为新的白内障药物研发提供最新的参考。
Cataracts remain the leading cause of blindness globally. They manifest as lens opacification triggered by various factors, leading to blurred vision. In severe cases, patients may eventually lose their vision entirely. There are many types of cataracts, and their pathogenesis has not been fully clarified. Currently, oxidative stress is widely acknowledged as the primary influencing factor. Pharmacological intervention remains a significant clinical challenge in cataract management. At present, there are no drugs on the market capable of truly reversing cataracts; existing medications can only alleviate the progression of the condition to a certain extent. Surgical treatment remains the only effective approach at this stage. However, economic limitations and the risks of postoperative complications hinder its accessibility for certain patient groups. The treatment of cataracts has consistently been a research hotspot in the field of ophthalmology. Current research mainly centers on two strategic approaches: optimizing surgical techniques alongside improved perioperative pharmaceutical regimens to minimize complications, and conducting basic researches on disease mechanisms to facilitate drug discovery. Effective drug treatment has long been a major gap in current clinical treatment. In recent years, significant progress has been achieved in the exploration of cataract mechanisms and the development of new drugs. Despite the remarkable advancements in uncovering cataract pathogenesis and identifying novel therapeutic targets in recent years, substantial challenges remain in translating these discoveries into clinically applicable medications. This article reviews the progress in mechanism research, the current state of pharmacological interventions, and the clinical research developments of several promising cataract drugs, aiming to provide the latest reference for the research and development of new cataract drugs.

文章亮点

1. 关键发现

 • 通过系统地分析白内障发病机制、药物治疗及临床研究现状，发现白内障有望实现真正意义上的药物治疗。

2. 已知与发现

 • 目前白内障的发病机制尚未研究透彻，主要侧重于晶状体的氧化损伤、晶状体上皮细胞凋亡、蛋白质聚集和沉淀等方向。现有的白内障药物仅能在一定程度上延缓疾病的进展。随着临床研究的不断深入，白内障的药物治疗迎来了新的希望。

3. 意义与改变

 • 随着机制研究的深入和临床转化的推进，白内障药物治疗将有望从当前辅助性、延缓性的角色，发展成为有效的临床治疗选择。

       白内障是全球第一大致盲性眼病。研究报告指出，2020年50岁及以上人群失明的主要原因是白内障[1]。白内障导致的失明人数约1 701万例，占全球失明人数的39.55%。8 348万人因白内障而出现中度和重度视力障碍，占全球的28.30%[2]。目前手术仍是白内障治疗唯一的有效手段，与高收入国家相比，中低收入国家承担的负担更大，视力结局更差[3-4]。白内障常见类型包括年龄相关性白内障（age-related cataracts, ARC）、并发性白内障、外伤性白内障、代谢性白内障等。
       白内障是晶状体发生病变导致的。晶状体主要由晶状体囊、上皮细胞、晶状体皮质和晶状体核构成[5]。晶状体的功能体现在其屈光特性，能将图像聚焦在视网膜上，多个部位共同参与维持其透明度[6]。然而，由于多种原因，如年龄增长、遗传因素、眼部外伤、长期暴露于紫外线、空气污染、糖尿病等[7-9]，晶状体的蛋白质发生变性和混浊导致光线散射，图像无法正常聚焦。晶状体不溶性蛋白持续增多还会导致晶状体增大、阻碍房水回流从而进一步影响视神经导致失明。白内障的发病机制目前尚未完全阐明，氧化应激是当前最主流的学说[10]。
       目前还没有能够有效逆转白内障的上市药物，现有的药物治疗仅能在一定程度上延缓白内障的进展。本文旨在对白内障的发病机制、四类主要的治疗药物现状以及相关的临床药物研究进展进行综述，并对未来的白内障药物治疗前景进行展望。

1 白内障的机制研究

       白内障的影响因素较多，发病机制也较为复杂，至今仍需要不断探索。现有的机制研究侧重于晶状体的氧化损伤、晶状体上皮细胞凋亡、蛋白质聚集和沉淀等方向。这些机制为药物研发提供了多个潜在的靶点。
       普遍认为晶状体的氧化损伤是白内障形成的主要原因。活性氧（reactive oxygen species, ROS）作为重要的细胞内信号分子，在多种生理功能调节中均发挥关键作用[11]。ROS易在眼睛受到外界刺激或多种代谢途径中产生，而高水平的ROS导致氧化损伤，特别是在包括晶状体在内的眼前部区域[12]。氧化损伤还会引起晶状体蛋白的变性，甚至作用于DNA而导致基因突变等，最终诱发白内障[12-13]。大量研究发现，脂质过氧化在晶状体老化过程中积累，可能推动白内障的进展。有动物研究显示，晶状体中谷胱甘肽过氧化物酶4（glutathione peroxidase 4, GPX4）缺乏会导致脂质过氧化增加，进而引发晶状体质膜损伤和早发性白内障[14]。脂质过氧化抑制剂的给药可以显著减轻白内障的形成，这为先天性白内障的研究与治疗提供了新的方向。
       晶状体上皮细胞凋亡被认为是非先天性白内障的共同病理机制。可能由细胞外或细胞自主刺激触发。目前研究的凋亡途径主要通过内质网应激诱导[15]和线粒体功能障碍介导[16]。Liu等[17]研究发现，C/EBP（CCAAT/enhancer-binding protein, CCAAT/增强子结合蛋白）的同源蛋白CHOP（C/EBP homologous protein）通过与TRB3（Tribbles homolog 3, Tribbles同源物3）启动子结合促进TRB3的表达，引发内质网应激，导致晶状体上皮细胞中的线粒体功能障碍和细胞凋亡，加速白内障的发展。Tian等[18]研究发现，ATF4（activating transcription factor 4, 激活转录因子4）-ATF3（activating transcription factor 3, 激活转录因子3）-CHOP通路在KLF6（Krüppel-like factor 6, Krüppel样因子6）诱导的晶状体上皮细胞凋亡中起重要作用。Wang等[19]研究发现，FABP3（Fatty acid-binding protein 3, 脂肪酸结合蛋白3）能够通过调节晶状体上皮细胞铁死亡来促进细胞凋亡和氧化应激，这些均可能成为白内障的潜在治疗靶点。
       晶状体内不溶性蛋白质的增加是白内障的典型特征，预防乃至逆转晶状体蛋白的聚集和沉淀是近年来的重要研究方向。晶状体中存在3种类型的晶状体蛋白：α-晶状体蛋白、β-晶状体蛋白和γ-晶状体蛋白[20-21]，后两者为结构蛋白，α-晶状体蛋白还兼具分子伴侣的功能[22-24]。Khan等[25]通过系统研究发现，γ-晶状体蛋白聚积会导致Rho/ROCK（Rho-associated coiled-coil kinase, Rho相关卷曲螺旋蛋白激酶）、TGF-β（transforming growth factor-β, 转化生长因子-β）、Wnt/β-catenin（wingless/integrated β-catenin，Wnt/β-连环蛋白）、NF-κB（nuclear factor κB，核因子κB）和PI3K（phosphatidylinositol-3-kinase, 磷脂酰肌醇3-激酶）-AKT（protein kinase B, 蛋白激酶B）-mTOR（mammalian target of rapamycin, 哺乳动物雷帕霉素靶蛋白）等信号通路异常，进而诱发白内障。Hao等[26]在冬眠动物眼睛晶状体中研究发现一种特殊适应机制：泛素-蛋白酶体系统（ubiquitin-proteasome system, UPS），能够促进聚集的晶状体蛋白溶解，且其中的关键蛋白E3泛素连接酶（E3 ubiquitin ligase, RNF114）在人类晶状体中也能发挥类似作用。这一研究为开发新的白内障治疗方法提供了潜在思路。
       基因层面，最新的荟萃分析梳理了与ARC相关的多个基因和生物途径[27]，为ARC的遗传学研究提供了重要的参考。该团队确定了101个与白内障相关的独立全基因组遗传位点，包括57个从未报道过的。确定了4种基因： GNL3（guanine nucleotide binding protein-like 3, 鸟嘌呤核苷酸结合蛋白样3）、JAG1（Jagged1, 齿状蛋白1）、METTL21A（methyltransferase like 21A, 甲基转移酶样蛋白21A）和CREB1（cAMP responsive element binding protein 1, 反应结合蛋白1）与8种药物具有药物-基因相互作用[27]。研究进一步证实了1型糖尿病与白内障风险之间的因果关系，强调了血糖控制的重要性。同时，JAG1基因与氢化可的松的相互作用提示皮质类固醇可能具有抗白内障潜力[28]。
       此外还有基于蛋白质组学改变和相应的信号通路[29]以及基因突变导致的先天性白内障[30]等机制研究。但由于白内障类型多样，影响因素复杂，国内外科学家对其机制的探索仍在不断进行中。

2 药物治疗现状

2.1 抗氧化应激

       在ARC的发展过程中，氧化应激会导致晶状体成分的生化改变[31-32]，严重白内障患者的房水样本中往往具有较低的抗氧化能力[33]。这些都表明抗氧化能力下降在白内障的形成和进展中起重要作用。因此，抗氧化剂和ROS清除剂对白内障具有潜在的治疗作用[34]。目前市面上应用的抗氧化剂主要包括膳食抗氧化剂以及具有抗氧化作用的药物[10]。下面主要介绍3种典型的抗氧化剂及其应用。
       膳食抗氧化剂主要包括多种维生素、叶黄素和玉米黄质等，多项研究均证实其在抗氧化应激上的价值，以及在延缓白内障进展上的作用[10,21]。以叶黄素为例，其作为一种强抗氧化剂，在预防和改善多种年龄相关性疾病上发挥一定的作用[35-36]。同时，叶黄素具有过滤蓝光的功能，能够在预防和改善白内障方面发挥作用[37]。临床研究显示，叶黄素的摄入和患白内障的风险呈负相关[38-40]。这类膳食抗氧化剂可以从食物或药品中获取，主要用于保护视力和延缓疾病的进程。
       谷胱甘肽（glutathione, GSH）是主要的非酶类抗氧化剂，主要以还原型存在，参与人体内的多种氧化还原过程[41]。晶状体内含有较高浓度的GSH，以抵御氧化损伤并维持正常功能[42-43]。但随着年龄增长，人体内尤其是晶状体内的GSH水平不断下降，无法有效抵御氧化损伤的发生。这一机制被广泛认为是ARC形成的重要因素[44]。临床上，谷胱甘肽滴眼液主要用于初期ARC的治疗。
       除GSH外，游离氨基酸也具有显著的抗氧化能力，且在晶状体中具有较高的浓度[45]。牛磺酸是晶状体中主要的氨基酸，在抗氧化应激环节中发挥着重要作用[46]。动物研究表明牛磺酸对高血糖诱导的晶状体病变具有保护作用[47]。牛磺酸的抗氧化作用还表现在它可以提高晶状体中Na+、K+-ATP酶和Ca2+-ATP酶的活性、稳定细胞膜[48]。补充牛磺酸可保护晶状体免受GSH消耗导致的氧化损伤，进而延缓白内障的形成[46]。有研究者指出，牛磺酸和GSH水平降低是导致先天性白内障病理表型的最主要代谢驱动因素[49]。市面上的牛磺酸滴眼液主要用于牛磺酸代谢失调引起的白内障。

2.2 醌型学说药物

       1957年荻野提出醌型学说，认为晶状体内色氨酸、酪氨酸等氨基酸代谢异常会导致醌型化合物的生成，醌型化合物属于芳香族化合物，具有难溶于水的特性。这类化合物可以和β-晶状体蛋白和γ-晶状体蛋白的巯基结合进而形成有色的不溶性蛋白，进而出现白内障[50]。醌型化合物也被用于诱导ARC的产生。竞争性地抑制其与晶状体蛋白的巯基组合，可以保持晶状体的透明度[51]。目前，市面上的代表药物为吡诺克辛滴眼液，适用于初期ARC。虽然疗效存在争议，但Phit 等[50]通过对多年来体内外的临床研究分析，分别从机制和临床疗效上初步评价了吡诺克辛对白内障的治疗价值，肯定了其对晶状体蛋白的抗氧化作用，但在减慢或逆转晶状体皮质混浊以及对包括眩光、对比敏感度在内的图像质量改善效果上均需进一步研究。

2.3 醛糖还原酶抑制剂

       多元醇途径是高血糖患者晶状体产生氧化应激的主要因素[52]。醛糖还原酶（aldose reductase, AR）是多元醇途径的关键酶，可以将葡萄糖和半乳糖分别还原成山梨醇和半乳糖醇[53]。体内长时间的高血糖状态会激活多元醇代谢途径，导致糖醇聚集[54-55]。这一理论在糖尿病性白内障及其他并发症的发展及治疗中起重要作用，但更多相关信号通路仍在不断探索中[56-57]。AR抑制剂能够抑制AR的活性，减少糖醇的生成。Trevor等[58]探索使用机器学习筛选AR抑制剂治疗糖尿病性白内障，以发现更多的潜在药物。筛选结果具有较高的参考价值，模型预测的几种药物已被广泛研究用于治疗白内障，包括瑞舒伐他汀、地奥司美丁、依折麦布等。目前AR抑制剂已知的代表药物有苄达赖氨酸滴眼液、法可林滴眼液等，但部分药物在临床疗效仍存在争议。

2.4 中药

       陈曦等[59]在对中医古籍中内障疾病的研究中发现，古籍中记载的内障疾病主要包括绿风内障、青风内障和圆翳内障等。中医临床常采用化痰补虚、清肝解郁、化痰活血、滋阴降火平肝等治疗策略。目前市面上有一些针对白内障的中成药，如障眼明片、石斛夜光丸、金花明目丸等，可用于早中期的ARC治疗。
       除了对白内障的预防和延缓作用外，中医药的价值还体现在对白内障患者的术后调理上。Liu等[60]在相关综述中指出，多种中药方剂对视力具有改善和恢复作用，多种中药成分对ARC具有潜在治疗价值，同时肯定了包括针灸和中药熏蒸在内的多种中医疗法的临床价值。

3 国内外新药研发现状

       目前，手术治疗仍是白内障治疗最有效的手段，但是高昂的手术费以及可能出现的多种术后并发症仍是普通家庭面临的一大负担。市面上的白内障药物主要用于延缓病情进展，基于抗氧化应激的药物研发仍是国内外新药研发的重要方向，包括典型的抗氧化剂、氨基酸类和多种植物来源的抗氧化剂等，部分药物在体内外白内障模型中均表现出一定的潜力[61]。
       N-乙酰肌肽（N-acetyl-carnosine, NACS）作为L-肌肽（l-carnosine, LCS）的前药，被证实能在一定程度上改善视力[62]。LCS可以清除ROS并防止其诱导的分子损伤。2004年一项关于1% NACS滴眼液的临床研究就已经展现了其临床价值，该研究中65例白内障老年患者经过短期治疗后，视力和眩光敏感性有所改善。且几乎所有患者对该药耐受性良好，试验过程中并未发现全身或眼部的不良反应[63]。同样，2006年一项针对犬白内障的局部抗氧化药物研究使用包括NACS在内的局部抗氧化剂制剂，晶状体混浊略有减少[64]。也有临床研究表明，NACS眼液可改善糖尿病眼部并发症患者的ARC和视力[65-66]。一项将NACS进行剂型改变的研究，发现固体脂质纳米颗粒可以对药物的角膜渗透、安全性和稳定性产生积极影响[67]，为后期的临床研究奠定了基础。但NACS对白内障真正的逆转作用还有待深入研究。
       一项随机、双盲、安慰剂对照的多中心1/2期临床试验，评估了2.6% EDTA（ethylenediaminetetraacetic acid disodium, 乙二胺四乙酸二钠）眼科溶液对早期ARC患者视觉功能的改善效果。研究纳入了41只眼，从对比敏感度、晶状体密度、安全性与耐受性角度展现了2.6% EDTA滴眼液的潜在价值[68]。但目前该研究结果还存在一定的争议性，需要更多后续研究来共同验证该结论的可靠性[69-70]。EDTA作为一种钙螯合剂，已被证实可以减少晶状体中的氧化应激和炎症级联反应，该眼科溶液通过添加甲磺酰甲烷（methylsulfonylmethane, MSM）作为渗透增强剂，显著提高了EDTA在眼内组织包括晶状体中的传递效率[71]。
       错误折叠的晶状体蛋白聚集是不同类型白内障的常见原因。错误折叠的蛋白质改变了晶状体蛋白的相互作用，并显著降低了晶状体蛋白的溶解度和稳定性，从而促进蛋白质聚集和晶状体混浊。目前，基于晶状体蛋白聚集溶解机制的抗白内障药物已成为白内障新药研发的一大重要方向[21]。
       研究发现，羊毛甾醇合成酶（lanosterol synthase, LSS）是新的白内障致病基因，其合成产物羊毛甾醇可逆转晶状体蛋白的异常聚集[72]。随后，在对大鼠和食蟹猴的白内障动物模型中同样证实了羊毛甾醇对晶状体混浊的抑制作用[73,74]。润尔眼科正在开展一项针对早中期ARC患者的药物临床研究，采用羊毛甾醇前药分子进行局部滴眼治疗。该产品通过增加羊毛甾醇的可溶解性和稳定性，使局部应用后房水中的药物浓度增加，显著提升了对白内障的防治效果，已经获得相关化合物发明专利。这是白内障药物研发的一大重要突破，是全球首个靶向作用于晶状体上皮细胞的白内障新药。也有国外研究者发现一种包含天然类固醇的滴眼液能够消除小鼠白内障的部分蛋白质团块[75]。这些基于类固醇化合物的研究进展，表明对氧甾醇类药物进行结构改造是颇具前景的非手术治疗方向，有望在不久的将来实现药物治愈白内障的目标。
       白内障药物市场巨大，全球关于白内障治疗药物的基础研究也是百花齐放。多种植物来源的提取物在白内障的治疗研究中也展现其特有的价值。有研究者发现，藏红花可改善动脉粥样硬化诱导的新西兰白兔的白内障病变[76]。慈姑多糖提取物在大鼠白内障模型中可显著改善晶状体混浊和病理变化，其机制可能与调节Nrf2（nuclear factor erythroid 2-related factor 2, 核因子红系2相关因子2）/ERS（endoplasmic reticulum stress, 内质网应激）介导的细胞凋亡来预防ARC有关[77]。白藜芦醇作为一种天然多酚，能够通过清除自由基发挥抗氧化抗衰老的作用，对晶状体具有治疗和预防作用[78]。白藜芦醇在动物模型中展现出对糖尿病性白内障以及ARC患者的保护作用[79-81]。这些研究都为其用于预防或延缓白内障的发展提供了潜在证据价值，值得进行更深入的研究。
       由于眼睛生理结构的特殊性，眼部治疗药物新剂型的研发也在不断探索中。传统的全身给药途径难以保证在眼内尤其是晶状体内达到有效的药物浓度，眼表局部给药也需克服重重的眼内屏障[82]。晶体发育过程中上皮细胞不断增殖、迁移并分化为次级纤维细胞，逐步沉积在晶状体中心形成晶状体核和晶状体皮质[5]。其结构上的致密性导致药物在晶状体内分布较为缓慢，使得药物难以发挥预期作用。目前，已有纳米载体技术应用于白藜芦醇的药物设计，增强其抗氧化应激效果[81,83]。Wang等[84]通过将活性抗氧化物表没食子儿茶素没食子酸酯与锌离子配位，构建抗氧化纳米粒子，提升生物利用度与多通路抗氧化能力，在白内障大鼠模型中表现出良好的效果。此外，通过对药物化学结构进行修饰以提高眼内药物浓度的研究也在进行中。

4 总结与展望

       白内障的机制探索及靶点药物研究为白内障的药物治疗开辟了新的方向。尽管目前能真正有效治疗白内障的药物仍存在较大缺口，但已经有多种白内障治疗药物进入临床研究阶段，新靶点、新剂型的创新药物也不断被研发出来。在不久的将来，具有真正治疗意义的白内障药物将走向市场，造福患者。

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1、复旦大学上海医学院“青年临床科学家培养计划”。
The work was supported by Shanghai Medical College Fudan University “Young Clinical Scientist Training Program”.The work was supported by Shanghai Medical College Fudan University “Young Clinical Scientist Training Program”. ( )
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发布于: 2022-12-01
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