The Eye Hospital, School of Ophthalmology & Optometry, Wenzhou Medical University, Wenzhou, 325027, China; Oujiang Laboratory (Zhejiang Lab for Regenerative Medicine Vision and Brain Health), Wenzhou, Zhejiang, 325000, China.
Oujiang Laboratory (Zhejiang Lab for Regenerative Medicine Vision and Brain Health), Wenzhou, Zhejiang, 325000, China; School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Eur J Med Chem. 2024 Dec 15;280:116933. doi: 10.1016/j.ejmech.2024.116933. Epub 2024 Oct 1.
For clinically prevalent traumatic optic neuropathy (TON) and other retinal and optic nerve injuries lacking effective therapeutic agents, there is an urgent clinical demand for developing highly efficient and safe neuroprotective agents. Here, we have integrated naturally sourced chalcone with isatin through a catalyst-free green synthesis method, reporting a series of spirocyclic chalcone derivatives with significantly lower cytotoxicity than chalcone itself. Following in vitro cell protection assays in models of hydrogen peroxide and glutamic acid-induced damage, multiple active compounds capable of combating both forms of damage were identified. Among these, candidate compound X38 demonstrated promising neuroprotective prospects: in vitro, it attenuated glutamate-induced cell apoptosis, while in vivo, it effectively ameliorated retinal thinning and loss of optic nerve electrophysiological function induced by optic nerve injury. Preliminary mechanistic studies suggest that X38 exerts its neuroprotective effects by mitigating intracellular ROS accumulation, inhibiting JNK phosphorylation, and alleviating oxidative stress. Additionally, acute toxicity studies (intraperitoneal injection, 500 mg/kg) underscored the favorable in vivo safety profile of X38. Taken together, this study has designed a class of safe, neuroprotective spirocyclic chalcone derivatives that can be synthesized using green methods, offering an attractive candidate for treating retinal and optic nerve injuries.
对于临床上普遍存在的创伤性视神经病变(TON)和其他缺乏有效治疗药物的视网膜和视神经损伤,迫切需要开发高效、安全的神经保护剂。在这里,我们通过无催化剂的绿色合成方法将天然来源的查尔酮与靛红结合,报告了一系列具有比查尔酮本身更低细胞毒性的螺环查尔酮衍生物。在过氧化氢和谷氨酸诱导损伤的体外细胞保护试验后,鉴定出多种能够对抗两种损伤形式的活性化合物。在这些化合物中,候选化合物 X38 表现出有希望的神经保护前景:体外,它减轻了谷氨酸诱导的细胞凋亡,而体内,它有效改善了视神经损伤引起的视网膜变薄和视神经电生理功能丧失。初步的机制研究表明,X38 通过减轻细胞内 ROS 积累、抑制 JNK 磷酸化和缓解氧化应激来发挥其神经保护作用。此外,急性毒性研究(腹腔注射,500mg/kg)强调了 X38 在体内的良好安全性。综上所述,本研究设计了一类安全的、具有神经保护作用的螺环查尔酮衍生物,可以通过绿色方法合成,为治疗视网膜和视神经损伤提供了有吸引力的候选药物。