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光生物调节抑制糖尿病视网膜病变的长期结构和功能损伤。

Photobiomodulation Inhibits Long-term Structural and Functional Lesions of Diabetic Retinopathy.

机构信息

Department of Medicine, Case Western Reserve University, Cleveland, OH.

Department of Ophthalmology, Second Hospital of Jilin University, Changchun, Jilin, China.

出版信息

Diabetes. 2018 Feb;67(2):291-298. doi: 10.2337/db17-0803. Epub 2017 Nov 22.

Abstract

Previous studies demonstrated that brief (3 to 4 min) daily application of light at 670 nm to diabetic rodents inhibited molecular and pathophysiologic processes implicated in the pathogenesis of diabetic retinopathy (DR) and reversed diabetic macular edema in small numbers of patients studied. Whether or not this therapy would inhibit the neural and vascular lesions that characterize the early stages of the retinopathy was unknown. We administered photobiomodulation (PBM) therapy daily for 8 months to streptozotocin-diabetic mice and assessed effects of PBM on visual function, retinal capillary permeability, and capillary degeneration using published methods. Vitamin D receptor and transcripts were quantified by quantitative real-time PCR, and the abundance of c-Kit stem cells in blood and retina were assessed. Long-term daily administration of PBM significantly inhibited the diabetes-induced leakage and degeneration of retinal capillaries and also significantly inhibited the diabetes-induced reduction in visual function. PBM also inhibited diabetes-induced reductions in retinal mRNA levels and numbers of circulating stem cells (CD45/c-Kit), but these effects may not account for the beneficial effects of PBM on the retinopathy. PBM significantly inhibits the functional and histopathologic features of early DR, and these effects likely are mediated via multiple mechanisms.

摘要

先前的研究表明,每天对糖尿病啮齿动物进行 3 至 4 分钟的 670nm 光短时间照射,可抑制糖尿病视网膜病变(DR)发病机制中涉及的分子和病理生理过程,并在少数研究患者中逆转糖尿病性黄斑水肿。这种疗法是否会抑制视网膜病变早期特征的神经和血管病变尚不清楚。我们对链脲佐菌素诱导的糖尿病小鼠进行了每日光生物调节(PBM)治疗 8 个月,并使用已发表的方法评估 PBM 对视觉功能、视网膜毛细血管通透性和毛细血管变性的影响。通过定量实时 PCR 定量维生素 D 受体和 转录物的丰度,并评估血液和视网膜中 c-Kit 干细胞的丰度。长期每日 PBM 治疗可显著抑制糖尿病引起的视网膜毛细血管渗漏和变性,也可显著抑制糖尿病引起的视觉功能下降。PBM 还可抑制糖尿病引起的视网膜 mRNA 水平和循环干细胞(CD45/c-Kit)数量的减少,但这些作用可能不能解释 PBM 对视网膜病变的有益作用。PBM 可显著抑制早期 DR 的功能和组织病理学特征,这些作用可能通过多种机制介导。

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