BackgroundTo determine whether photobiomodulation (PBM) rescued the disruption of Na+/Ca2+ homeostasis and mitochondrial membrane potential by ouabain; the Na, K-ATPase inhibitor. For PBM in this study, a 660 nm LED array was used at energy densities of 0.78, 1.56, 3.12, 6.24, and 9.36 J/cm2.ResultsHCN-2 neuronal cells treated with ouabain showed loss of cell polarity, disrupted cell morphology, and decreased cell viability, which were improved after PBM treatment. We found that ouabain-induced Na, K-ATPase inhibition promoted activation of downstream signaling through Src, Ras, and mitogen-activated protein kinase (MAPK), which were suppressed after PBM treatment. This provided evidence of Na, K-ATPase α-subunit inactivation and intracellular Ca2+ increase. In response to ouabain, we observed activation of Src and MAPK by Na, K-ATPase, decreased mitochondrial membrane potential, and Na+-dependent Ca2+ increases, which were restored by PBM treatment.ConclusionsThis study demonstrated that Na+/K+ imbalance could be regulated by PBM treatment in neuronal cells, and we suggest that PBM is a potential therapeutic tool for Na, K-ATPase targeted neuronal diseases.

中文翻译：

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光生物调节疗法对哇巴因神经元损伤的影响：Na、K-ATPase的调节；源代码；和丝裂原活化蛋白激酶信号通路

背景确定光生物调节 (PBM) 是否挽救了哇巴因对 Na+/Ca2+ 稳态和线粒体膜电位的破坏；Na, K-ATPase 抑制剂。对于本研究中的 PBM，使用能量密度为 0.78、1.56、3.12、6.24 和 9.36 J/cm2 的 660 nm LED 阵列。结果用哇巴因处理的 HCN-2 神经元细胞显示出细胞极性丧失、细胞形态破坏和细胞活力降低，PBM 处理后改善。我们发现哇巴因诱导的 Na、K-ATPase 抑制通过 Src、Ras 和丝裂原活化蛋白激酶 (MAPK) 促进下游信号的激活，这些在 PBM 处理后被抑制。这提供了 Na、K-ATPase α-亚基失活和细胞内 Ca2+ 增加的证据。作为对哇巴因的反应，我们观察到 Na、K-ATPase、