Department of Neuroscience and Regenerative Medicine, Medical College of Georgia, Augusta University, 1120 15th Street, Augusta, GA, 30912, USA.
J Mol Neurosci. 2018 Aug;65(4):514-526. doi: 10.1007/s12031-018-1121-3. Epub 2018 Jul 22.
Photobiomodulation (PBM) has been demonstrated as a neuroprotective strategy, but its effect on perinatal hypoxic-ischemic encephalopathy is still unknown. The current study was designed to shed light on the potential beneficial effect of PBM on neonatal brain injury induced by hypoxia ischemia (HI) in a rat model. Postnatal rats were subjected to hypoxic-ischemic insult, followed by a 7-day PBM treatment via a continuous wave diode laser with a wavelength of 808 nm. We demonstrated that PBM treatment significantly reduced HI-induced brain lesion in both the cortex and hippocampal CA1 subregions. Molecular studies indicated that PBM treatment profoundly restored mitochondrial dynamics by suppressing HI-induced mitochondrial fragmentation. Further investigation of mitochondrial function revealed that PBM treatment remarkably attenuated mitochondrial membrane collapse, accompanied with enhanced ATP synthesis in neonatal HI rats. In addition, PBM treatment led to robust inhibition of oxidative damage, manifested by significant reduction in the productions of 4-HNE, P-H2AX (S139), malondialdehyde (MDA), as well as protein carbonyls. Finally, PBM treatment suppressed the activation of mitochondria-dependent neuronal apoptosis in HI rats, as evidenced by decreased pro-apoptotic cascade 3/9 and TUNEL-positive neurons. Taken together, our findings demonstrated that PBM treatment contributed to a robust neuroprotection via the attenuation of mitochondrial dysfunction, oxidative stress, and final neuronal apoptosis in the neonatal HI brain.
光生物调节（PBM）已被证明是一种神经保护策略，但它对围产期缺氧缺血性脑病的影响尚不清楚。本研究旨在探讨 PBM 对缺氧缺血（HI）诱导的新生大鼠脑损伤的潜在有益作用。出生后的大鼠接受缺氧缺血性损伤，随后通过 808nm 连续波二极管激光进行为期 7 天的 PBM 治疗。我们证明 PBM 治疗显著减轻了 HI 诱导的皮质和海马 CA1 区的脑损伤。分子研究表明，PBM 治疗通过抑制 HI 诱导的线粒体碎片化，显著恢复了线粒体动力学。对线粒体功能的进一步研究表明，PBM 治疗显著减轻了线粒体膜崩溃，伴随着新生 HI 大鼠中 ATP 合成的增强。此外，PBM 治疗导致氧化损伤的强烈抑制，表现为 4-HNE、P-H2AX（S139）、丙二醛（MDA）和蛋白质羰基的产生显著减少。最后，PBM 治疗通过减少促凋亡级联 3/9 和 TUNEL 阳性神经元，抑制 HI 大鼠中依赖线粒体的神经元凋亡的激活。总之，我们的研究结果表明，PBM 治疗通过减轻新生 HI 大脑中的线粒体功能障碍、氧化应激和最终神经元凋亡，为神经保护做出了贡献。
