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A Protocol for Transcranial Photobiomodulation Therapy in Mice
Published on: November 18, 2018
Bmal1 regulates hippocampal oxidative damage in cognitive memory impairment induced by artificial light at night in
Ting Lei1, Jie Xia1, Huiying Du1
1Department of Environmental Health, School of Public Health, China Medical University, Shenyang, Liaoning 110122, China; Key Laboratory of Environmental Stress and Chronic Disease Control & Prevention (China Medical University), Ministry of Education, Shenyang, Liaoning 110122, China.
Abstract:
Artificial light at night (ALAN) has emerged as a significant public health concern, yet its effects on cognitive impairment remain poorly understood. This study investigated the impact of 28 consecutive days of 5-lx ALAN exposure on hippocampal function in C57BL/6 J mice. We evaluated locomotor behavior, neuronal morphology, neurogenesis, oxidative stress, and circadian rhythms, revealing that ALAN induces cognitive impairment. ALAN exposure reduced Bmal1 expression, increased reactive oxygen species (ROS) and malondialdehyde accumulation, and disrupted the time-of-day-dependent differences expression of NRF2, SOD1, and GPX1. These alterations suppressed SOD and GPX enzymatic activity, leading to hippocampal oxidative damage. To clarify BMAL1's role, we used adeno-associated virus (AAV) to modulate Bmal1 expression in the hippocampus. ALAN increased hippocampal apoptosis, which was exacerbated by Bmal1 knockdown and mitigated by its overexpression. These findings suggest that ALAN can contribute to memory impairment by disrupting hippocampal damage and impairing neurogenesis through its effect on Bmal1. This study identifies potential molecular targets for preventing and treating cognitive impairment and neurodegenerative disorders.
