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A Protocol for Transcranial Photobiomodulation Therapy in Mice
Published on: November 18, 2018
Low-level laser therapy regulates microglial function through Src-mediated signaling pathways: implications for
Sheng Song1, Feifan Zhou, Wei R Chen
1MOE Key Laboratory of Laser Life Science & Institute of Laser Life Science, College of Biophotonics, South China Normal University, No, 55 Zhongshan Avenue West, Guangzhou, Tianhe District, 510631, China.
Background:
Activated microglial cells are an important pathological component in brains of patients with neurodegenerative diseases. The purpose of this study was to investigate the effect of He-Ne (632.8 nm, 64.6 mW/cm2) low-level laser therapy (LLLT), a non-damaging physical therapy, on activated microglia, and the subsequent signaling events of LLLT-induced neuroprotective effects and phagocytic responses.
Methods:
To model microglial activation, we treated the microglial BV2 cells with lipopolysaccharide (LPS). For the LLLT-induced neuroprotective study, neuronal cells with activated microglial cells in a Transwell™ cell-culture system were used. For the phagocytosis study, fluorescence-labeled microspheres were added into the treated microglial cells to confirm the role of LLLT.
Results:
Our results showed that LLLT (20 J/cm2) could attenuate toll-like receptor (TLR)-mediated proinflammatory responses in microglia, characterized by down-regulation of proinflammatory cytokine expression and nitric oxide (NO) production. LLLT-triggered TLR signaling inhibition was achieved by activating tyrosine kinases Src and Syk, which led to MyD88 tyrosine phosphorylation, thus impairing MyD88-dependent proinflammatory signaling cascade. In addition, we found that Src activation could enhance Rac1 activity and F-actin accumulation that typify microglial phagocytic activity. We also found that Src/PI3K/Akt inhibitors prevented LLLT-stimulated Akt (Ser473 and Thr308) phosphorylation and blocked Rac1 activity and actin-based microglial phagocytosis, indicating the activation of Src/PI3K/Akt/Rac1 signaling pathway.
Conclusions:
The present study underlines the importance of Src in suppressing inflammation and enhancing microglial phagocytic function in activated microglia during LLLT stimulation. We have identified a new and important neuroprotective signaling pathway that consists of regulation of microglial phagocytosis and inflammation under LLLT treatment. Our research may provide a feasible therapeutic approach to control the progression of neurodegenerative diseases.
Insights
Low-level laser therapy (LLLT) reduces inflammation and enhances microglial phagocytosis in neurodegenerative disease models. This therapy activates Src, a key signaling molecule, to suppress inflammatory responses and promote debris clearance, offering a potential therapeutic strategy.
Area of Science:
- Neuroscience
- Cell Biology
- Biomedical Engineering
Background:
- Activated microglia are implicated in neurodegenerative disease pathology.
- Low-level laser therapy (LLLT) is a non-damaging physical therapy with potential therapeutic applications.
- Investigating LLLT's effects on microglia is crucial for understanding neuroprotection.
Purpose of the Study:
- To examine the impact of He-Ne LLLT on activated microglia.
- To elucidate LLLT-induced signaling pathways involved in neuroprotection.
- To assess LLLT's influence on microglial phagocytic responses.
Main Methods:
- Microglial activation was induced using lipopolysaccharide (LPS) in BV2 cells.
- A Transwell™ system modeled neuroprotection with neuronal and microglial cells under LLLT.
- Fluorescence-labeled microspheres quantified LLLT's effect on microglial phagocytosis.
Main Results:
- LLLT (20 J/cm²) attenuated toll-like receptor (TLR)-mediated inflammation by down-regulating cytokine expression and nitric oxide (NO) production.
- LLLT activated tyrosine kinases Src and Syk, inhibiting MyD88-dependent signaling.
- Src activation enhanced Rac1 activity and F-actin accumulation, promoting microglial phagocytosis via the Src/PI3K/Akt/Rac1 pathway.
Conclusions:
- Src plays a critical role in LLLT-mediated suppression of inflammation and enhancement of phagocytosis in activated microglia.
- A novel neuroprotective signaling pathway involving microglial phagocytosis and inflammation regulation by LLLT was identified.
- LLLT presents a promising therapeutic approach for managing neurodegenerative disease progression.
