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首页> 外文期刊>The Journal of Biochemistry >Involvement of interleukin 18 in cataract development in hereditary cataract UPL rats.
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Involvement of interleukin 18 in cataract development in hereditary cataract UPL rats.

机译:白细胞介素18参与遗传性白内障UPL大鼠白内障的发展。

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摘要

Our previous studies have demonstrated that lens epithelial damage by excessive nitric oxide causes an elevation in lens opacification in UPL rats, and it has been reported that interferon-gamma production in lens epithelial cells is involved in cataract development. In this study, we investigated the involvement of interleukin (IL)-18, which leads to interferon-gamma, in UPL rat lenses. The opacification of UPL rat lenses starts at 39 days of age. The gene expression levels causing IL-18 activation (IL-18, IL-18 receptor and caspase-1) are increased at 32 days of age, and the expression of mature IL-18 protein in the UPL rat lenses also increases with ageing. On the other hand, the interferon-gamma levels in UPL rat lenses are increased, and the increase in interferon-gamma levels in UPL rat lenses reaches a maximum at 39 days of age. Mature IL-18 expression and interferon-gamma production are achieved prior to the onset of lens opacification. In conclusion, the expression levels of IL-18 in the lenses of UPL rats are increased with aging. In addition, interferon-gamma levels in the lenses of UPL rats are also increased. It is possible that interferon-gamma generated by the activated IL-18 may induce cataract development in UPL rats.
机译:我们以前的研究表明,过量一氧化氮对晶状体上皮的损害会引起UPL大鼠晶状体混浊的升高,并且据报道晶状体上皮细胞中干扰素-γ的产生与白内障发展有关。在这项研究中,我们调查了UPL大鼠晶状体中白细胞介素(IL)-18的参与,后者导致干扰素-γ。 UPL大鼠晶状体的混浊从39日龄开始。导致IL-18激活的基因表达水平(IL-18,IL-18受体和caspase-1)在32天龄时增加,并且随着年龄的增长,UPL大鼠晶状体中成熟IL-18蛋白的表达也增加。另一方面,UPL大鼠晶状体中干扰素-γ水平增加,UPL大鼠晶状体中干扰素-γ水平的增加在39天时达到最大值。在晶状体混浊开始之前就已经达到成熟的IL-18表达和γ干扰素产生。总之,UPL大鼠晶状体中IL-18的表达水平随年龄增加而增加。此外,UPL大鼠晶状体中的干扰素-γ水平也增加。活化的IL-18产生的干扰素-γ可能会诱导UPL大鼠出现白内障。

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