Aksar Arzu Toruk, Yuksel Nursen, Gok Mustafa, Cekmen Mustafa, Caglar Yusuf
Department of Ophthalmology, Kocaeli University Faculty of Medicine, Kocaeli 41200, Turkey.
Department of Ophthalmology, Ministry of Health-Ordu University Research and Training Hospital, Ordu 52000, Turkey.
Int J Ophthalmol. 2015 Apr 18;8(2):239-44. doi: 10.3980/j.issn.2222-3959.2015.02.05. eCollection 2015.
To evaluate the neuroprotective activity of systemically administered edaravone in early and late stage of experimental glaucoma in rats.
In this study, 60 Wistar albino rats were used. Experimental glaucoma model was created by injecting hyaluronic acid to the anterior chamber once a week for 6wk in 46 of 60 subjects. Fourteen subjects without any medication were included as control group. Edaravone administered intraperitoneally 3 mg/kg/d to the 15 of 30 subjects starting at the onset of glaucoma induction and also administered intraperitoneally 3 mg/kg/d to the other 15 subjects starting at three weeks after the onset of glaucoma induction. The other 16 subjects who underwent glaucoma induction was administered any therapy. Retinal ganglion cells (RGCs) have been marked with dextran tetramethylrhodamine (DTMR) retrograde at the end of the sixth week and after 48h, subjects were sacrificed by the method of cardiac perfusion. Alive RGC density was assessed in the whole-mount retina. Whole-mount retinal tissues homogenized and nitric oxide (NO), malondialdehyde (MDA) and total antioxidant capacity (TAC) values were measured biochemically.
RGCs counted with Image-Pro Plus program, in the treatment group were found to be statistically significantly protected, compared to the glaucoma group (Bonferroni, P<0.05). The neuroprotective activity of edaravone was found to be more influential by administration at the start of the glaucoma process. Statistically significant lower NO levels were determined in the glaucoma group comparing treatment groups (Bonferroni, P<0.05). MDA levels were found to be highest in untreated glaucoma group, TAC levels were found to be lower in the glaucoma induction groups than the control group (Bonferroni, P<0.05).
Systemic administration of Edaravone in experimental glaucoma showed potent neuroprotective activity. The role of oxidative stress causing RGC damage in glaucoma was supported by this study results.
评估全身给药依达拉奉对大鼠实验性青光眼早期和晚期的神经保护活性。
本研究使用60只Wistar白化大鼠。在60只大鼠中的46只中，通过每周一次向前房注射透明质酸，持续6周来建立实验性青光眼模型。14只未接受任何药物治疗的大鼠作为对照组。30只大鼠中的15只在青光眼诱导开始时腹腔注射依达拉奉3mg/kg/d，另外15只在青光眼诱导开始三周后腹腔注射依达拉奉3mg/kg/d。另外16只接受青光眼诱导的大鼠未接受任何治疗。在第六周结束时，用葡聚糖四甲基罗丹明（DTMR）逆行标记视网膜神经节细胞（RGCs），48小时后，通过心脏灌注法处死大鼠。在全层视网膜中评估存活RGC密度。将全层视网膜组织匀浆，生化测定一氧化氮（NO）、丙二醛（MDA）和总抗氧化能力（TAC）值。
与青光眼组相比，使用Image-Pro Plus程序计数治疗组中的RGCs，发现具有统计学显著的保护作用（Bonferroni检验，P<0.05）。发现依达拉奉在青光眼过程开始时给药的神经保护活性更具影响力。与治疗组相比，青光眼组中NO水平在统计学上显著降低（Bonferroni检验，P<0.05）。发现未治疗的青光眼组中MDA水平最高，青光眼诱导组中的TAC水平低于对照组（Bonferroni检验，P<0.05）。
全身给药依达拉奉在实验性青光眼中显示出强大的神经保护活性。本研究结果支持氧化应激在青光眼导致RGC损伤中的作用。
