Yan Huan, Peng Yanli, Huang Wei, Gong Liyan, Li Li
Department of Ophthalmology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China.
Chongqing Aier-Mega Eye Hospital, Aier Eye Hospital Group, Chongqing 400060, China.
J Ophthalmol. 2017;2017:7205408. doi: 10.1155/2017/7205408. Epub 2017 Oct 2.
To investigate whether B-crystallin protects against acute retinal ischemic reperfusion injury (I/R) and elucidate the potential antioxidant mechanisms. Retinal I/R injury was made by elevating the intraocular pressure (IOP) 110 mmHg for 60 min, and B-crystallin (1 × 10 g/L) or vehicle solution was administered intravitreously immediately after I/R injury. The animal was sacrificed 24 h, 1 w, and 1 m after the I/R injury. The retina damage was detected by hematoxylin and eosin (HE) staining and electroretinography (ERG). The level of malondialdehyde (MDA), nitric oxide (NO), and the total superoxide dismutase (T-SOD) was determined. An immunohistochemical study was performed to detect the activation of inducible nitric oxide synthase (iNOS) and NF- (nuclear factor-) kappaB (NF-B) p65. The decrease of retinal thickness and the number of retinal ganglion cells (RGCs) can be suppressed by B-crystallin. And the amplitudes of a- and b-wave were remarkably greater without B-crystallin. Similarly, B-crystallin also significantly decreased the level of MDA and NO and enhanced the activities of T-SOD. The positive expression of iNOS and NF-kappaB p65 was obviously reduced while treated with B-crystallin. B-crystallin can inhibit the expression of NF-B and its antioxidative effect to protect the retina from I/R injury.
探讨β-晶状体蛋白是否能保护免受急性视网膜缺血再灌注损伤（I/R）并阐明潜在的抗氧化机制。通过将眼压升高至110 mmHg持续60分钟造成视网膜I/R损伤，在I/R损伤后立即玻璃体内注射β-晶状体蛋白（1×10 g/L）或溶剂溶液。在I/R损伤后24小时、1周和1个月处死动物。通过苏木精和伊红（HE）染色及视网膜电图（ERG）检测视网膜损伤。测定丙二醛（MDA）、一氧化氮（NO）水平及总超氧化物歧化酶（T-SOD）活性。进行免疫组织化学研究以检测诱导型一氧化氮合酶（iNOS）和核因子-κB（NF-κB）p65的激活情况。β-晶状体蛋白可抑制视网膜厚度的减少及视网膜神经节细胞（RGCs）数量的减少。并且在没有β-晶状体蛋白时，a波和b波的振幅明显更大。同样，β-晶状体蛋白也显著降低MDA和NO水平并增强T-SOD活性。在用β-晶状体蛋白处理时，iNOS和NF-κB p65的阳性表达明显降低。β-晶状体蛋白可抑制NF-κB的表达并通过其抗氧化作用保护视网膜免受I/R损伤。
