Department of Ophthalmology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, P. R. China.
Hunan Key Laboratory of Ophthalmology, Changsha, Hunan, 410008, P. R. China.
Adv Sci (Weinh). 2024 Nov;11(41):e2407043. doi: 10.1002/advs.202407043. Epub 2024 Sep 4.
Glaucoma is an irreversible blinding eye disease characterized by retinal ganglion cell (RGC) death.Previous studies have demonstrated that protecting mitochondria and activating the CaMKII/CREB signaling pathway can effectively protect RGC and axon. However, currently treatments are often unsatisfactory, and the pathogenesis of glaucoma requires further elucidation. In this study, a ROS-responsive dual drug conjugate (OLN monomer) is first designed that simultaneously bonds nicotinamide and oleic acid. The conjugate self-assembled into nanoparticles (uhOLN-NPs) through the aggregation of multiple micelles and possesses ROS scavenging capability. Then, a polymer with a hypoxic response function is designed, which encapsulates uhOLN-NPs to form nanoparticles with hypoxic and ROS responses (HOLN-NPs). Under hypoxia in RGCs, the azo bond of HOLN-NPs breaks and releases uhOLN-NPs. Meanwhile, under high ROS conditions, the thioketone bond broke, leading to the dissociation of nano-prodrug. The released nicotinamide and oleic acid co-scavenge ROS and activate the CaMKII/CREB pathway, protecting mitochondria in RGCs. HOLN-NPs exhibit a significantly superior protective effect on R28 cells in glutamate models of glaucoma. The accumulation of HOLN-NPs in retinal RGCs lead to significant inhibition of RGC apoptosis and axonal damage in vivo. Notably, HOLN-NPs provide a new therapeutic approach for patients with neurodegenerative disease.
青光眼是一种不可逆的致盲眼病,其特征是视网膜神经节细胞 (RGC) 死亡。先前的研究表明,保护线粒体并激活 CaMKII/CREB 信号通路可以有效保护 RGC 和轴突。然而,目前的治疗方法往往不尽如人意,青光眼的发病机制需要进一步阐明。在这项研究中,首次设计了一种 ROS 响应性双药物偶联物(OLN 单体),该偶联物同时键合烟酰胺和油酸。该偶联物通过多个胶束的聚集自组装成纳米颗粒(uhOLN-NPs),并具有 ROS 清除能力。然后,设计了一种具有缺氧响应功能的聚合物,该聚合物包裹 uhOLN-NPs 形成具有缺氧和 ROS 响应的纳米颗粒(HOLN-NPs)。在 RGC 缺氧的情况下,HOLN-NPs 的偶氮键断裂并释放 uhOLN-NPs。同时,在高 ROS 条件下,硫酮键断裂,导致纳米前药解离。释放的烟酰胺和油酸共同清除 ROS 并激活 CaMKII/CREB 通路,保护 RGC 中的线粒体。HOLN-NPs 在谷氨酸诱导的青光眼 R28 细胞模型中表现出明显优越的保护作用。HOLN-NPs 在视网膜 RGC 中的积累导致体内 RGC 凋亡和轴突损伤的显著抑制。值得注意的是,HOLN-NPs 为神经退行性疾病患者提供了一种新的治疗方法。