阿尔茨海默症(Alzheimer′s disease, AD)的药物疗效欠佳, 单色光照射治疗是候选方案之一。本文综述了开展的单色光治疗AD的细胞模型研究。β淀粉样蛋白(amyloid-β protein, Aβ)或过氧化氢可诱导体外培养的神经细胞凋亡。发光二极管红光(640±15 nm)(RLED640)照射能够降低Aβ25-35诱导的PC12细胞凋亡, 抑制过氧化氢诱导的分化PC12细胞凋亡, 它们分别由cAMP和酪氨酸羟化酶所介导。Tau蛋白功能缺失可用秋水仙素模拟。用秋水仙素和过氧化氢共同孵育可致分化PC12细胞流产凋亡, 用RLED640照射能够抑制这种凋亡。节律紊乱可以用肿瘤坏死因子α来模拟。研究发现, 低强度810 nm激光照射可以拮抗肿瘤坏死因子α诱导的NIH3T3成纤维细胞时钟基因表达抑制。

Alzheimer’s disease (AD) is now the most common neurodegenerative disease. As drugs approved are not very effective, the brain-mediated monochromatic phototherapy is one of therapeutic candidate approaches. The cellular model studies of AD have been conducted in our laboratory and will be reviewed in this paper. Genetic studies have shown that dysfunction of amyloid-β (Aβ) or tau is sufficient to cause AD. Aβ or hydrogen peroxide (H2O2) induced neuron apoptosis might be a cellular model of AD. We found red light at 640±15 nm from light emitting diode array (RLED640) might inhibit PC12 cell apoptosis induced by Aβ25-35 and apoptosis of differentiated PC12 cell (dPC12) induced by H2O2, which might be mediated by cAMP and tyrosine hydroxylase, respectively. The dysfunction of tau might be mimicked by colchicine. We found H2O2 and colchicines might lead to dPC12 abortive apoptosis, and the abortive apoptosis might be inhibited with RLED640. The rhythm dysfunction in AD might be mimicked by tumor necrosis factor α(TNF-α). We also found low intensity 810 nm laser irradiation might rehabilitate inhibition of circadian gene expression of NIH 3T3 fibroblasts induced by the TNF-α.