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OA
Photobiomodulation Attenuates Form-Deprivation Myopia Progression in Mice through a Dopamine-Signaling Cascade
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.
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 retina 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.
李俊宇;郭好运;申琪
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||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||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||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
生物科学
光生物调控治疗多巴胺近视巩膜视网膜色素上皮细胞
photobiomodulation therapydopaminemyopiascleraretinal pigment epithelium
《激光生物学报》 2026 (2)
185-192,8
国家自然科学基金资助项目(62305119)广东省自然科学基金资助项目(2023A1515011489,2025A1515011522)广东省科学技术协会资助项目(SKXRC2025015).
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