Photobiomodulation inhibits retinal degeneration in diabetic mice through modulation of stem cell mobilization and gene expression

IF 3 2区 医学 Q1 OPHTHALMOLOGY
Jingyan Ge , Yinan Zhang , Ling Han , Liangliang Zhao , Hongwei Zhao , Dan Qiao , Yan Cheng
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Abstract

The number of people suffering from type 2 diabetes (DM2) is increasing and over 30 percent of DM2 patients will develop diabetic retinopathy (DR). Available therapeutic approaches for DR have their limitations. It is of great significance to search for other effective alternate therapeutic approaches. The present study aimed to explore the beneficial effects of photobiomodulation (PBM) on the diabetic retinopathy and underlying mechanisms. Streptozotocin was administered to male mice to establish diabetic model. The mice in the diabetic group (DM) received no treatment, and the mice in DM + PBM group received LED illumination (wavelength 670 nm) once a day for 20 consecutive weeks. Retinal vessel degenerate changes, the expression levels of E-Cadherin, N-Cadherin and the mRNA levels of c-kit, CXCR4, MYPT1, SCF, SDF1-α in retina, the levels of SDF-1α and SCF in the peripheral blood and the number of LSK cells expressing c-kit and sca-1 were determined. PBM could significantly inhibit the degenerative change of diabetic retinal vessels, decrease the expression levels of E-Cadherin and N-Cadherin and the mRNA levels of c-kit, CXCR4, MYPT1, SCF, SDF1-α and increase VEGF mRNA levels in retina. PBM could also increase the levels of SDF-1α and SCF in the peripheral blood and the number of LSK cells expressing c-kit and sca-1 in diabetic mice. PBM at 4 min/day for 20 consecutive weeks significantly inhibit the degenerative change of diabetic retinal vessels, and PBM is likely to produce its beneficial effects on the retina through promoting the migration of bone marrow stem cells to circulation and diabetic retinal tissue. The present study provides a new therapeutic direction and experimental foundation for the treatment of diabetic retinopathy.
光生物调节通过调节干细胞动员和基因表达抑制糖尿病小鼠视网膜变性。
2型糖尿病(DM2)患者的数量正在增加,其中超过30%的DM2患者将发展为糖尿病视网膜病变(DR)。DR的现有治疗方法有其局限性。寻找其他有效的替代治疗方法具有重要意义。本研究旨在探讨光生物调节(PBM)对糖尿病视网膜病变的有益作用及其机制。采用链脲佐菌素建立雄性小鼠糖尿病模型。糖尿病组(DM)小鼠不进行任何治疗,DM+PBM组小鼠接受LED照明(波长670nm),每天1次,连续20周。检测大鼠视网膜血管变性变化,视网膜E-Cadherin、N-Cadherin表达水平及c-kit、CXCR4、MYPT1、SCF、SDF1-α mRNA水平,外周血SDF-1α、SCF水平及表达c-kit、SCF -1的LSK细胞数量。PBM能显著抑制糖尿病视网膜血管的退行性改变,降低E-Cadherin、N-Cadherin的表达水平以及c-kit、CXCR4、MYPT1、SCF、SDF1-α mRNA水平,升高VEGF mRNA水平。PBM还能增加糖尿病小鼠外周血中SDF-1α和SCF的水平以及表达c-kit和sca-1的LSK细胞的数量。连续20周,4分钟/天的PBM显著抑制糖尿病视网膜血管的退行性改变,PBM可能是通过促进骨髓干细胞向循环和糖尿病视网膜组织的迁移来产生其对视网膜的有益作用。本研究为糖尿病视网膜病变的治疗提供了新的治疗方向和实验基础。
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来源期刊
Experimental eye research
Experimental eye research 医学-眼科学
CiteScore
6.80
自引率
5.90%
发文量
323
审稿时长
66 days
期刊介绍: The primary goal of Experimental Eye Research is to publish original research papers on all aspects of experimental biology of the eye and ocular tissues that seek to define the mechanisms of normal function and/or disease. Studies of ocular tissues that encompass the disciplines of cell biology, developmental biology, genetics, molecular biology, physiology, biochemistry, biophysics, immunology or microbiology are most welcomed. Manuscripts that are purely clinical or in a surgical area of ophthalmology are not appropriate for submission to Experimental Eye Research and if received will be returned without review.
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