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A Protocol for Transcranial Photobiomodulation Therapy in Mice
Published on: November 18, 2018
Low-level light in combination with metabolic modulators for effective therapy of injured brain
Tingting Dong1, Qi Zhang1, Michael R Hamblin1
1Department of Dermatology, Harvard Medical School, Wellman Center for Photomedicine, Massachusetts General Hospital, Boston, Massachusetts, USA.
Abstract:
Vascular damage occurs frequently at the injured brain causing hypoxia and is associated with poor outcomes in the clinics. We found high levels of glycolysis, reduced adenosine triphosphate generation, and increased formation of reactive oxygen species and apoptosis in neurons under hypoxia. Strikingly, these adverse events were reversed significantly by noninvasive exposure of injured brain to low-level light (LLL). Low-level light illumination sustained the mitochondrial membrane potential, constrained cytochrome c leakage in hypoxic cells, and protected them from apoptosis, underscoring a unique property of LLL. The effect of LLL was further bolstered by combination with metabolic substrates such as pyruvate or lactate both in vivo and in vitro. The combinational treatment retained memory and learning activities of injured mice to a normal level, whereas other treatment displayed partial or severe deficiency in these cognitive functions. In accordance with well-protected learning and memory function, the hippocampal region primarily responsible for learning and memory was completely protected by combination treatment, in marked contrast to the severe loss of hippocampal tissue because of secondary damage in control mice. These data clearly suggest that energy metabolic modulators can additively or synergistically enhance the therapeutic effect of LLL in energy-producing insufficient tissue-like injured brain.
Insights
Low-level light (LLL) therapy reverses brain injury-induced hypoxia, neuronal apoptosis, and cognitive deficits. Combining LLL with metabolic substrates like pyruvate or lactate offers significant neuroprotection and restores memory and learning functions.
Area of Science:
- Neuroscience
- Biochemistry
- Photomedicine
Background:
- Brain injury frequently causes vascular damage, leading to hypoxia.
- Hypoxia in injured brain tissue results in impaired energy metabolism, increased oxidative stress, and neuronal apoptosis.
- These pathological changes are linked to poor clinical outcomes.
Purpose of the Study:
- To investigate the therapeutic potential of low-level light (LLL) in mitigating hypoxia-induced brain damage.
- To explore the synergistic effects of combining LLL with metabolic substrates (pyruvate or lactate) for enhanced neuroprotection.
- To evaluate the impact of these treatments on cognitive functions, specifically learning and memory.
Main Methods:
- In vitro and in vivo models of hypoxic brain injury.
- Assessment of cellular energy metabolism, mitochondrial function, and apoptosis.
- Evaluation of cognitive performance (learning and memory) in mice.
- Histological analysis of hippocampal tissue.
Main Results:
- LLL exposure reversed hypoxia-induced glycolysis, reduced adenosine triphosphate generation, and decreased reactive oxygen species and apoptosis in neurons.
- LLL sustained mitochondrial membrane potential and prevented cytochrome c leakage.
- Combination therapy with LLL and metabolic substrates (pyruvate or lactate) fully preserved learning and memory functions and protected hippocampal tissue in injured mice.
Conclusions:
- Low-level light therapy demonstrates significant neuroprotective effects against hypoxia-induced brain injury.
- Combining LLL with metabolic substrates like pyruvate or lactate synergistically enhances therapeutic efficacy.
- This combined approach offers a promising strategy for restoring cognitive function and preventing secondary brain damage.
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