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Antioxidant effects of LEDT in dystrophic muscle cells: involvement of PGC-1α and UCP-3 pathways
Guilherme Luiz da Rocha1, Dimitrius Santiago Passos Simões Fróes Guimarães1,2, Marcos Vinicius da Cruz1,2
1Department of Structural and Functional Biology, Institute of Biology, University of Campinas (UNICAMP), Campinas, SP, 13083-970862, Brazil.
Purpose:
Reactive oxygen species and mitochondrial dysfunction play a crucial role in the pathophysiology of Duchenne muscular dystrophy (DMD). The light-emitting diode therapy (LEDT) showed beneficial effects on the dystrophic muscles. However, the mechanisms of this therapy influence the molecular pathways in the dystrophic muscles, particularly related to antioxidant effects, which still needs to be elucidated. The current study provides muscle cell-specific insights into the effect of LEDT, 48 h post-irradiation, on oxidative stress and mitochondrial parameters in the dystrophic primary muscle cells in culture.
Methods:
Dystrophic primary muscle cells were submitted to LEDT, at multiple wavelengths (420 nm, 470 nm, 660 nm and 850 nm), 0.5 J dose, and evaluated after 48 h based on oxidative stress markers, antioxidant enzymatic system and biogenesis, and functional mitochondrial parameters.
Results:
The mdx muscle cells treated with LEDT showed a significant reduction of H2O2 production and 4-HNE, catalase, SOD-2, and GR levels. Upregulation of UCP3 was observed with all wavelengths while upregulation of PGC-1α and a slight upregulation of electron transport chain complexes III and V was only observed following 850 nm LEDT. In addition, the mitochondrial membrane potential and mitochondrial mass mostly tended to be increased following LEDT, while parameters like O2·- production tended to be decreased.
Conclusion:
The data shown here highlight the potential of LEDT as a therapeutic agent for DMD through its antioxidant action by modulating PGC-1α and UCP3 levels.
Insights
Light-emitting diode therapy (LEDT) reduces oxidative stress and improves mitochondrial function in Duchenne muscular dystrophy (DMD) muscle cells. This therapy shows potential for DMD treatment by enhancing antioxidant defenses and mitochondrial parameters.
Area of Science:
- Cell Biology
- Biomedical Engineering
- Genetics
Background:
- Reactive oxygen species and mitochondrial dysfunction are key factors in Duchenne muscular dystrophy (DMD) pathophysiology.
- Light-emitting diode therapy (LEDT) has demonstrated positive effects on dystrophic muscles, but its precise molecular mechanisms, especially antioxidant effects, require further investigation.
Purpose of the Study:
- To investigate the specific effects of LEDT on oxidative stress and mitochondrial parameters in primary muscle cells from DMD patients.
- To elucidate the molecular mechanisms underlying LEDT's therapeutic potential in DMD.
Main Methods:
- Primary muscle cells from mdx mice (a DMD model) were exposed to LEDT at various wavelengths (420, 470, 660, and 850 nm) with a 0.5 J dose.
- Cells were analyzed 48 hours post-irradiation for oxidative stress markers, antioxidant enzyme activity, biogenesis markers, and mitochondrial function.
Main Results:
- LEDT significantly reduced hydrogen peroxide (H2O2) production and levels of 4-HNE, catalase, SOD-2, and GR in mdx muscle cells.
- UCP3 was upregulated across all tested wavelengths, while PGC-1α and mitochondrial electron transport chain complexes (III and V) were upregulated specifically with 850 nm LEDT.
- LEDT generally increased mitochondrial membrane potential and mass, while decreasing superoxide (O2·-) production.
Conclusions:
- LEDT demonstrates therapeutic potential for Duchenne muscular dystrophy (DMD) by exerting antioxidant effects.
- The therapy modulates key molecular pathways, including PGC-1α and UCP3, suggesting a role in improving mitochondrial health and function in DMD.
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