正常衰老涉及大鼠视网膜和脉络膜中特定炎症标志物的调节。
Normal aging involves modulation of specific inflammatory markers in the rat retina and choroid.
作者信息
Steinle Jena J, Sharma Sheena, Smith Christopher P, McFayden-Ketchum Lisa S
机构信息
Department of Ophthalmology, University of Tennessee Health Science Center, 930 Madison Ave, Suite 722A, Memphis, TN 38163, USA.
出版信息
J Gerontol A Biol Sci Med Sci. 2009 Mar;64(3):325-31. doi: 10.1093/gerona/gln052. Epub 2009 Jan 30.
Recent work has suggested that inflammation is a common component of a number of age-related diseases. The hypothesis of the present study was that normal aging of the retina and choroid would increase levels of inducible nitric oxide synthase (iNOS), prostaglandin E2 (PGE2), and tumor necrosis factor alpha (TNF-alpha). To investigate this hypothesis, gene expression and protein analyses were completed on retinal and choroidal samples from Fischer 344 x Brown Norway F1 hybrid rats at 8, 22, and 32 months of age. Aging of the choroid produced significant increases in PGE2, with decreased TNF-alpha protein. Protein levels and messenger RNA of iNOS and TNF-alpha protein levels were significantly decreased in the aging retina in contrast to PGE2 protein activity, which was increased with age in the retina. These results suggest that PGE2 is likely involved in the aging process in both the retina and choroid, whereas iNOS plays a role predominantly in the retina.
近期研究表明，炎症是许多与年龄相关疾病的常见组成部分。本研究的假设是，视网膜和脉络膜的正常老化会增加诱导型一氧化氮合酶（iNOS）、前列腺素E2（PGE2）和肿瘤坏死因子α（TNF-α）的水平。为了验证这一假设，对8、22和32月龄的Fischer 344×Brown Norway F1杂交大鼠的视网膜和脉络膜样本进行了基因表达和蛋白质分析。脉络膜老化导致PGE2显著增加，而TNF-α蛋白减少。与视网膜中随年龄增加的PGE2蛋白活性相反，老化视网膜中iNOS的蛋白水平和信使核糖核酸以及TNF-α蛋白水平显著降低。这些结果表明，PGE2可能参与了视网膜和脉络膜的老化过程，而iNOS主要在视网膜中起作用。
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