Department of Ophthalmology, Shanghai Jiaotong University Affiliated Shanghai First People's Hospital, Shanghai, China.
Curr Eye Res. 2010 Oct;35(10):930-7. doi: 10.3109/02713683.2010.494820.
To investigate whether caffeic acid phenethyl ester (CAPE) has a protective effect on retinal ischemia/reperfusion (I/R) injury in rats, and to determine the possible antioxidant mechanisms.
Seventy-six female Wistar rats were randomized evenly into Sham, I/R injury model (M group), model plus vehicle (MV), and model plus CAPE (MC) groups. Retinal ischemia/reperfusion injury was induced by increasing the intraocular pressure to 110 mmHg for 60 min. Rats in the MV and MC groups were injected with vehicle and CAPE (10 µmol/kg i.p.), respectively, before reperfusion and once a day for one or seven days after I/R. The levels of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) in the retinal tissues were determined 24 hr after I/R. Retinal cells apoptosis was detected 24 hr after I/R injury by terminal deoxynucleotidyl transferase-mediated digoxigenin-dUTP nick-end labeling staining. On day 7 after reperfusion, the electroretinogram (ERG) was recorded, and the retinal histology was examined and quantified using light microscopy.
CAPE significantly decreased the MDA levels and increased the activities of SOD, GSH-Px, and CAT in the retina compared with the ischemia group (p< 0.05). CAPE attenuated the I/R-induced apoptosis of retinal cells in the inner nuclear and ganglion cells of the rat retina. CAPE also suppressed the I/R-induced reduction in the a- and b-wave amplitudes of the ERG (p<0.05). The thickness of the entire retina, inner nuclear layer, and inner plexiform layer and the number of cells in the ganglion cell layer in the MC group were significantly greater than those in the M group (p<0.05).
CAPE can protect the rat retina from I/R injury by enhancing the antioxidation ability and inhibiting the apoptosis of retinal cells, which suggests that CAPE is potentially useful for treating I/R-induced eye disorders.
研究咖啡酸苯乙酯（CAPE）对大鼠视网膜缺血/再灌注（I/R）损伤是否具有保护作用，并确定其可能的抗氧化机制。
76 只雌性 Wistar 大鼠随机均分为假手术（Sham）组、I/R 损伤模型（M 组）、模型加载体（MV）组和模型加 CAPE（MC）组。通过升高眼内压至 110mmHg 持续 60min 诱导视网膜 I/R 损伤。MV 和 MC 组大鼠分别在再灌注前和 I/R 后每天腹腔注射载体和 CAPE（10µmol/kg）。I/R 后 24h 测定视网膜组织丙二醛（MDA）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）和过氧化氢酶（CAT）水平。I/R 损伤后 24h 通过末端脱氧核苷酸转移酶介导的地高辛-dUTP 缺口末端标记法检测视网膜细胞凋亡。再灌注后第 7 天记录视网膜电图（ERG），并通过光镜检查和量化视网膜组织学。
与缺血组相比，CAPE 可显著降低 MDA 水平，增加视网膜 SOD、GSH-Px 和 CAT 的活性（p<0.05）。CAPE 可减轻 I/R 诱导的大鼠视网膜内核和节细胞层视网膜细胞凋亡。CAPE 还可抑制 I/R 引起的 ERG 的 a 波和 b 波幅度降低（p<0.05）。MC 组的整个视网膜、内核层和内丛状层的厚度以及节细胞层的细胞数均明显大于 M 组（p<0.05）。
CAPE 通过增强抗氧化能力和抑制视网膜细胞凋亡，可保护大鼠视网膜免受 I/R 损伤，提示 CAPE 可能有助于治疗 I/R 引起的眼部疾病。
