Institute of Advanced Materials for Nano-Bio Applications, School of Ophthalmology and Optometry, Wenzhou Medical University, Wenzhou, China.
Henan Provincial People's Hospital and People's Hospital of Henan University, Henan Eye Institute, Henan Eye Hospital, Zhengzhou, China.
Mol Vis. 2021 Jul 8;27:438-456. eCollection 2021.
To examine the neuroprotective effect of minocycline on retinal ischemia-reperfusion (IR) injury in rats and investigate its possible mechanism of action.
Retinal IR injury was established by increasing the intraocular pressure in rats up to 110 mmHg for 60 min. The animals with retinal IR injury were intraperitoneally injected with 22.5 mg/kg minocycline twice a day for 14 days. The control group received the same amount of saline. Subsequently, funduscopic examination, retinal thickness measurement, retinal microvascular morphology, full-field electroretinography (ERG), retinal apoptotic cell count, and remaining retinal ganglion cell (RGC) count were performed. The expression of iNOS, Bax, Bcl2, IL-1α, IL-6, TNF-α, caspase-3, GFAP, Iba-1, Hif-1α, and Nrf2 was examined with real-time PCR and western blotting.
Minocycline treatment prevented IR-induced rat retinal edema and retinal cells apoptosis at the early stage and alleviated retina atrophy, blood vessel tortuosity, functional photoreceptor damage, and RGC degeneration at the late stage of the IR injury. At the molecular level, minocycline affected retinal gene and protein expression induced by IR.
The results suggested that minocycline has a neuroprotective effect on rat retinal IR injury, possibly through anti-inflammation, antiapoptosis, antioxidation, and inhibition of microglial activation.
探讨米诺环素对大鼠视网膜缺血再灌注（IR）损伤的神经保护作用，并探讨其可能的作用机制。
通过将大鼠眼内压升高至 110mmHg 持续 60min 建立视网膜 IR 损伤模型。将发生视网膜 IR 损伤的动物每天两次腹腔内注射 22.5mg/kg 米诺环素，共 14 天。对照组给予等量生理盐水。随后进行眼底检查、视网膜厚度测量、视网膜微血管形态学、全视野视网膜电图（ERG）、视网膜细胞凋亡计数和剩余视网膜神经节细胞（RGC）计数。采用实时 PCR 和 Western blot 检测 iNOS、Bax、Bcl2、IL-1α、IL-6、TNF-α、caspase-3、GFAP、Iba-1、Hif-1α 和 Nrf2 的表达。
米诺环素治疗可预防 IR 诱导的大鼠视网膜水肿和视网膜细胞早期凋亡，并减轻视网膜萎缩、血管扭曲、功能感光细胞损伤和 RGC 变性等晚期 IR 损伤。在分子水平上，米诺环素影响了 IR 诱导的视网膜基因和蛋白表达。
结果表明，米诺环素对大鼠视网膜 IR 损伤具有神经保护作用，可能通过抗炎、抗细胞凋亡、抗氧化和抑制小胶质细胞激活来实现。
