光生物调控通过多巴胺信号级联反应抑制小鼠形觉剥夺性近视进展

李俊宇, 郭好运, 申 琪

激光生物学报 ›› 2026, Vol. 35 ›› Issue (2) : 185-192.

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激光生物学报 ›› 2026, Vol. 35 ›› Issue (2) : 185-192.
研究论文

光生物调控通过多巴胺信号级联反应抑制小鼠形觉剥夺性近视进展

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Photobiomodulation Attenuates Form-Deprivation Myopia Progression in Mice through a Dopamine-Signaling Cascade

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摘要

(1. 华南师范大学光电科学与工程学院,激光生命科学研究所暨激光生命科学教育部重点实验室,广州 510631;2. 华南师范大学光电科学与工程学院,广东省激光生命科学重点实验室,广州 510631)
摘  要:光生物调控治疗(PBMT)作为一种新兴的非药物物理干预手段,在近视防控中的应用前景受到广泛关注,但其最佳照射参数及潜在作用机制仍需进一步明确。本研究采用形觉剥夺近视(FDM)小鼠模型,通过设置不同功率密度的650 nm PBMT照射方案,系统评估PBMT对近视相关眼轴增长的抑制作用,并检测视网膜中多巴胺(DA)与一氧化氮(NO)水平变化,同时,在长时程干预条件下对疗效与安全性进行验证,并结合离体细胞试验探讨DA的下游分子响应。结果显示:PBMT可显著抑制FDM小鼠眼轴异常增长(P<0.05),其中功率密度为0.25 mW/cm2时眼轴抑制效果最为显著;PBMT可显著促进视网膜DA与NO分泌升高(P<0.05),并呈剂量依赖性变化;长时程PBMT在近视形成过程中能够稳定抑制眼轴增长,而对正常小鼠眼轴无明显影响,提示其具备一定安全性潜力;进一步研究发现,DA可上调视网膜上皮细胞中细胞Fos原癌基因(c-Fos)表达并促进金属蛋白酶组织抑制剂2(TIMP2)基因表达,该效应在D1R抑制条件下被削弱,提示DA-D1R介导的c-Fos/TIMP2相关通路可能参与PBMT抑制眼轴增长的过程。研究表明,PBMT能够有效缓解FDM小鼠近视进展,其作用可能与激活视网膜DA/NO信号并调控组织重塑相关分子网络有关,这为红光近视干预的参数优化与机制研究提供了试验依据。
关键词:光生物调控治疗;多巴胺;近视;巩膜;视网膜色素上皮细胞
中图分类号:Q935;R318.51                  文献标志码:A               DOI:10.3969/j.issn.1007-7146.2026.02.010

Abstract

Abstract: Photobiomodulation therapy (PBMT) has emerged as a promising non-pharmacological physical intervention for myopia control. However, the optimal irradiation parameters and the underlying mechanisms remain to be further clarified. In this study, a form-deprivation myopia (FDM) mouse model was established, and 650 nm PBMT protocols with different power densities were applied to systematically evaluate the inhibitory effect of PBMT on myopia-associated axial elongation. Changes in dopamine (DA) and nitric oxide (NO) levels in the retinal were quantified, and the efficacy and safety of long-term PBMT were further assessed. In addition, ex vivo cell experiments were performed to investigate downstream molecular responses to DA. The results showed that PBMT significantly suppressed abnormal axial elongation in FDM mice (P<0.05), with the most prominent effect observed at a power density of 0.25 mW/cm2. PBMT also markedly increased DA and NO secretion in the retinal (P<0.05) in a dose-dependent manner. Long-term PBMT stably inhibited axial elongation during myopia development without significantly affecting axial length in normal mice, suggesting a favorable safety profile. Furthermore, DA upregulated cellular FBJ osteosarcoma oncogene (c-Fos) expression and promoted tissue inhibitor of metalloproteinases (TIMP2) gene expression in retinal pigment epithelial cells, and these effects were attenuated by D1R inhibition, indicating that the DA-D1R-mediated c-Fos/TIMP2 pathway may contribute to PBMT-induced suppression of axial elongation. Collectively, these findings demonstrate that PBMT effectively alleviates myopia progression in FDM mice, potentially by activating retinal DA/NO signaling and modulating molecular networks associated with tissue remodeling, thereby providing experimental evidence for parameter optimization and mechanistic exploration of red-light-based myopia interventions.
Key words: photobiomodulation therapy; dopamine; myopia; sclera; retinal pigment epithelium
(Acta Laser Biology Sinica, 2026, 35(2): 185-192)

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李俊宇, 郭好运, 申 琪. 光生物调控通过多巴胺信号级联反应抑制小鼠形觉剥夺性近视进展[J]. 激光生物学报. 2026, 35(2): 185-192
LI Junyu, GUO Haoyun, SHEN Qi. Photobiomodulation Attenuates Form-Deprivation Myopia Progression in Mice through a Dopamine-Signaling Cascade[J]. Acta Laser Biology Sinica. 2026, 35(2): 185-192

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