Department of Ophthalmology, School of Medicine, Institute of Health Science, Gyeongsang National University, Jinju, Gyeongnam, Korea, Republic of Korea.
Curr Eye Res. 2010 Jul;35(7):657-63. doi: 10.3109/02713681003760143.
To investigate the effect of triamcinolone acetonide (TA) on retinal expression of decorin in a rat model of oxygen-induced retinopathy (OIR).
OIR was stimulated by exposing Sprague-Dawley (SD) rats to hyperoxia (80 +/- 1.3% O2) from postnatal day (P) 2 to P14 and then returning them to normoxia (room air, 21 +/- 1.5% O2). Control rats were maintained in normoxia. At P15, TA (40 mg/ml) was injected into the right vitreous of OIR rats and saline into the left vitreous of control rats. All rats were sacrificed at P18. RT-PCR, western blot and immunohistochemistry, TUNEL assay were performed to detect the effects of TA on molecular and morphological changes in retinal decorin levels in P18 OIR rats.
In P18 OIR rats, mRNA and protein of retinal levels and immunoreactivity of retinal decorin were significantly less (p-value = 0.0000000012, 0.0007, 0.000003; n = 5; respectively) than in control rats. In addition, neuronal cell death was increased in P18 OIR rats (p-value = 0.0028; n = 5) relative to controls. However, treatment with TA prevented the decrease of mRNA, protein levels, and immunoreactivity in retinal decorin in P18 OIR rats (p-value = 0.00023, 0.003, 0.000079; n = 5, respectively), and restored neuronal cell death in P18 OIR rats (p-value = 0.0022, n = 5).
Our results suggest that decorin is involved in hypoxic retinal damage and that TA protects retinal neurons damaged by relative hypoxia from decreased decorin levels.
研究曲安奈德（TA）对氧诱导视网膜病变（OIR）大鼠模型中视网膜decorin 表达的影响。
通过使 Sprague-Dawley（SD）大鼠在出生后第 2 天至第 14 天暴露于高氧（80±1.3%O2），然后将其恢复到常氧（室内空气，21±1.5%O2）来刺激 OIR。对照大鼠保持在常氧中。在 P15 时，将 TA（40mg/ml）注入 OIR 大鼠的右眼玻璃体，将生理盐水注入对照大鼠的左眼玻璃体。所有大鼠均在 P18 处死。进行 RT-PCR、western blot 和免疫组织化学、TUNEL 检测，以检测 TA 对 P18 OIR 大鼠视网膜 decorin 水平的分子和形态变化的影响。
在 P18 OIR 大鼠中，视网膜水平的 mRNA 和蛋白以及视网膜 decorin 的免疫反应性明显降低（p 值=0.0000000012、0.0007、0.000003；n=5；分别）比对照大鼠。此外，P18 OIR 大鼠的神经元细胞死亡增加（p 值=0.0028；n=5）与对照相比。然而，TA 治疗可防止 P18 OIR 大鼠视网膜 decorin 的 mRNA、蛋白水平和免疫反应性降低（p 值=0.00023、0.003、0.000079；n=5，分别），并恢复 P18 OIR 大鼠的神经元细胞死亡（p 值=0.0022，n=5）。
我们的结果表明 decorin 参与了缺氧性视网膜损伤，而 TA 可保护因相对缺氧而导致 decorin 水平降低的视网膜神经元。
