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首页> 外文期刊>Cellular Physiology and Biochemistry >Blocking IL-17A Alleviates Diabetic Retinopathy in Rodents
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Blocking IL-17A Alleviates Diabetic Retinopathy in Rodents

机译：阻断IL-17A减轻啮齿类动物的糖尿病性视网膜病变

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>Background/Aims: Interleukin (IL)-17A, a proinflammatory cytokine, has been implicated in several autoimmune diseases. However, it is unclear whether IL-17A is involved in diabetic retinopathy (DR), one of the most serious complications of autoimmune diabetes. This study aimed to demonstrate that IL-17A exacerbates DR by affecting retinal M??ller cell function. Methods: High glucose (HG)-treated rat M??ller cell line (rMC-1) was exposed to IL-17A, anti-IL-17A-neutralizing monoclonal antibody (mAb) or/and anti-IL-17 receptor (R)A-neutralizing mAb for 24 h. For in vivo study, DR was induced by intraperitoneal injections of streptozotocin (STZ). DR model mice were treated with anti-IL-17A mAb or anti-IL-17RA mAb in the vitreous cavity. Mice that were prepared for retinal angiography were sacrificed two weeks after intravitreal injection, while the rest were sacrificed two days after intravitreal injection. Results: IL-17A production and IL-17RA expression were increased in both HG-treated rMC-1 and DR retina. HG induced rMC-1 activation and dysfunction, as determined by the increased GFAP, VEGF and glutamate levels as well as the downregulated GS and EAAT1 expression. IL-17A exacerbated the HG-induced rMC-1 functional disorders, whereas either anti-IL-17A mAb or anti-IL-17RA mAb alleviated the HG-induced rMC-1 disorders. Intravitreal injections with anti-IL-17A mAb or anti-IL-17RA mAb in DR model mice reduced M??ller cell dysfunction, vascular leukostasis, vascular leakage, tight junction protein downregulation and ganglion cell apoptosis in the retina. Conclusions: IL-17A aggravates DR-like pathology at least partly by impairing retinal M??ller cell function. Blocking IL-17A is a potential therapeutic strategy for DR.
机译：> 背景/目标： 白细胞介素（IL）-17A是一种促炎性细胞因子，与多种自身免疫性疾病有关。但是，尚不清楚IL-17A是否参与糖尿病性视网膜病（DR），这是自身免疫性糖尿病最严重的并发症之一。这项研究旨在证明IL-17A通过影响视网膜M ?? ller细胞功能来加剧DR。 方法： 将高糖（HG）处理的大鼠M ?? ller细胞系（rMC-1）暴露于抗IL-17A中和性单克隆抗体IL-17A抗体（mAb）或/和抗IL-17受体（R）A中和单克隆抗体24小时。对于体内研究，DR是通过腹膜内注射链脲佐菌素（STZ）诱导的。用抗IL-17A mAb或抗IL-17RA mAb在玻璃体腔中治疗DR模型小鼠。玻璃体内注射后两周处死准备用于视网膜血管造影的小鼠，而玻璃体内注射后两天处死其余小鼠。 结果： HG处理的rMC-1和DR视网膜中IL-17A的产生和IL-17RA的表达均增加。 HG诱导的rMC-1激活和功能异常，这是由GFAP，VEGF和谷氨酸水平升高以及GS和EAAT1表达下调所决定的。 IL-17A加剧了HG诱导的rMC-1功能障碍，而抗IL-17A mAb或抗IL-17RA mAb均可缓解HG诱导的rMC-1功能障碍。在DR模型小鼠中玻璃体腔注射抗IL-17A mAb或抗IL-17RA mAb可以减少视网膜中M ?? ller细胞功能障碍，血管白细胞减少，血管渗漏，紧密连接蛋白下调和神经节细胞凋亡。 结论： IL-17A至少部分通过损害视网膜M ?? ller细胞功能来加重DR样病理。阻断IL-17A是DR的潜在治疗策略。

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