腺病毒介导BDNF基因转染对大鼠视神经损伤后视网膜中SOD、MDA水平的影响

Effect of Adenovirally Delivered Brain-derived Neurotrophic Factor on Superoxide Dismutase within the Retina of Experimentally Injured Optic Nerve of Rat Eyes

目的:腺病毒介导脑源性神经营养因子(Brain-derived neurotrophic factor,BDNF)转染对大鼠视神经损伤后视网膜中丙二醛(MDA)和超氧化物歧化酶(SOD)水平的影响。方法:建立大鼠视神经夹挫伤模型,随机分为BDNF腺病毒组、lac-Z腺病毒组和生理盐水组,将药物经玻璃体途径注射入大鼠眼内,并设正常大鼠对照。观察各组不同时间视网膜组织中MDA和SOD的含量变化。结果:正常SD大鼠视网膜组织MDA的含量为(5.21±1.32)nmol/ml,SOD的含量为(1751.57±180.55)U/g·pro。大鼠视神经夹伤后MDA含量升高,SOD含量降低。BDNF腺病毒组视网膜MDA含量为(6.67±1.36)nmol/ml(3d)、(5.72±1.66)nmol/ml(7d)、(5.54±1.03)nmol/ml(14d)and(5.33±1.45)nmol/ml(21d),低于两损伤对照组,而SOD含量为(158.55±173.39)U/g·pro(3d)、(161.24±184.57)U/g·pro(7d)、(1694.49±184.30)U/g·pro(14d)和(1721.75±179.86)U/g·pro(21d),高于两损伤对照组。在3 d、1 wk和2 wk时有显著统计学差异(P<0.05),两对照组间在各时间点均无统计学差异。结论:腺病毒介导BDNF转染对视神经损伤后视网膜损伤具有早期防护作用,其作用可能与BDNF刺激局部的SOD含量增加有关。眼科学报 2002;18:249-252.

Purpose: To study the changes of malondialdehyde(MDA) and superoxide dismutase (SOD) in the retinal tissues of the rats after optic nerve injury and the influence to it by adenovirally delivered brain-derived neurotrophic factor (BDNF) to ocular tissues. Methods: Adenovirus with BDNF gene, adenovirus with beta-galactosidase gene and balanced salt solution were injected, respectively, into vitreous of injured eyes of rat. The content of MDA and SOD in the retinal tissues of the rats were measured by means of quantity analysis in various time. That of normal retinal tissues were examined and used as control. Results: The content of MDA and SOD in the normal retina was (5. 33 ± 1. 45) nmol/ ml(21d), fewer than the two control groups' and the contents of SOD of BDNF group were (1587. 55 ± 173. 39) U/g · pro(3d). (1613. 24 ±184. 57) U/g · pro(7d). (1694. 49±184. 30) U/g · pro(14d) and (1721. 75 ±179. 86) U/g· pro(21d), more than the two control groups' meanwhile. There were significent differences at 3d, 1wk and 2wk( P < 0. 05). There were no significent differences between the two control groups at every time point. Conclusion: Adenovirally delivered BDNF to murine ocular tissues after optic nerve injury helps protect from oxidative stress during earlier period. The effect may be related to the increased amount of SOD within local tissue by BDNF. Eye Science 2002; 18: 249 - 252.