Department of Ophthalmology, Far Eastern Memorial Hospital, Banqiao Dist., New Taipei City 220, Taiwan.
Department of Electrical Engineering, Yuan Ze University, Chung-Li, Taoyuan 320, Taiwan.
Mar Drugs. 2020 Jan 27;18(2):83. doi: 10.3390/md18020083.
We investigated the therapeutic effects and related mechanisms of algae oil (ALG) to protect retinal ganglion cells (RGCs) in a rat model of anterior ischemic optic neuropathy (rAION).
Rats were daily gavaged with ALG after rAION induction for seven days. The therapeutic effects of ALG on rAION were evaluated using flash visual evoked potentials (FVEPs), retrograde labeling of RGCs, TUNEL assay of the retina, and ED1 staining of optic nerves (ONs). The levels of inducible nitric oxide synthase (iNOS), IL-1β, TNF-α, Cl-caspase-3, ciliary neurotrophic factor (CNTF), and p-ERK were analyzed by using western blots.
Protection of visual function in FVEPs amplitude was noted, with a better preservation of the P1-N2 amplitude in the ALG-treated group ( = 0.032) than in the rAION group. The density of RGCs was 2.4-fold higher in the ALG-treated group compared to that in the rAION group ( < 0.0001). The number of ED1-positive cells in ONs was significantly reduced 4.1-fold in the ALG-treated group compared to those in the rAION group ( = 0.029). The number of apoptotic RGCs was 3.2-fold lower in number in the ALG-treated group ( = 0.001) than that in the rAION group. The ALG treatment inhibited ERK activation to reduce the levels of iNOS, IL-1β, TNF-α, and Cl-caspase-3 and to increase the level of CNTF in the rAION model.
The treatment with ALG after rAION induction inhibits ERK activation to provide both anti-inflammatory and antiapoptotic effects in rAION.
我们研究了藻油（ALG）在大鼠前部缺血性视神经病变（rAION）模型中保护视网膜神经节细胞（RGC）的治疗效果及其相关机制。
rAION 诱导后，大鼠每天给予 ALG 灌胃治疗 7 天。通过闪光视觉诱发电位（FVEPs）、RGC 逆行标记、视网膜 TUNEL 检测和视神经（ON）ED1 染色评估 ALG 对 rAION 的治疗效果。采用 Western blot 分析诱导型一氧化氮合酶（iNOS）、IL-1β、TNF-α、Cl-caspase-3、睫状神经营养因子（CNTF）和 p-ERK 的水平。
FVEPs 振幅的视觉功能得到了保护，ALG 治疗组的 P1-N2 振幅保存更好（ = 0.032）。与 rAION 组相比，ALG 治疗组的 RGC 密度高 2.4 倍（ < 0.0001）。ON 中 ED1 阳性细胞的数量在 ALG 治疗组中减少了 4.1 倍（ = 0.029）。与 rAION 组相比，ALG 治疗组的 RGC 凋亡数量减少了 3.2 倍（ = 0.001）。ALG 治疗抑制 ERK 激活，降低 iNOS、IL-1β、TNF-α 和 Cl-caspase-3 的水平，增加 rAION 模型中的 CNTF 水平。
rAION 诱导后给予 ALG 治疗可抑制 ERK 激活，为 rAION 提供抗炎和抗凋亡作用。
