LED therapy plus idebenone treatment targeting calcium and mitochondrial signaling pathways in dystrophic muscle cells.

Autor: da Silva HNM; Department of Structural and Functional Biology, Institute of Biology, University of Campinas, Campinas, Brazil., Mizobuti DS; Department of Structural and Functional Biology, Institute of Biology, University of Campinas, Campinas, Brazil., Pereira VA; Department of Structural and Functional Biology, Institute of Biology, University of Campinas, Campinas, Brazil., da Rocha GL; Department of Structural and Functional Biology, Institute of Biology, University of Campinas, Campinas, Brazil., da Cruz MV; Department of Structural and Functional Biology, Institute of Biology, University of Campinas, Campinas, Brazil.; Obesity and Comorbidities Research Center (OCRC), Campinas, Brazil., de Oliveira AG; Department of Structural and Functional Biology, Institute of Biology, University of Campinas, Campinas, Brazil.; Obesity and Comorbidities Research Center (OCRC), Campinas, Brazil., Silveira LR; Department of Structural and Functional Biology, Institute of Biology, University of Campinas, Campinas, Brazil.; Obesity and Comorbidities Research Center (OCRC), Campinas, Brazil., Minatel E; Department of Structural and Functional Biology, Institute of Biology, University of Campinas, Campinas, Brazil. minatel@unicamp.br.
Jazyk: angličtina
Zdroj: Cell stress & chaperones [Cell Stress Chaperones] 2023 Nov; Vol. 28 (6), pp. 773-785. Date of Electronic Publication: 2023 Aug 14.
DOI: 10.1007/s12192-023-01369-2
Abstrakt: Intracellular calcium dysregulation, oxidative stress, and mitochondrial dysfunction are some of the main pathway contributors towards disease progression in Duchenne muscular dystrophy (DMD). This study is aimed at investigating the effects of light emitting diode therapy (LEDT) and idebenone antioxidant treatment, applied alone or together in dystrophic primary muscle cells from mdx mice, the experimental model of DMD. Mdx primary muscle cells were submitted to LEDT and idebenone treatment and evaluated for cytotoxic effects and calcium and mitochondrial signaling pathways. LEDT and idebenone treatment showed no cytotoxic effects on the dystrophic muscle cells. Regarding the calcium pathways, after LEDT and idebenone treatment, a significant reduction in intracellular calcium content, calpain-1, calsequestrin, and sarcolipin levels, was observed. In addition, a significant reduction in oxidative stress level markers, such as H 2 O 2 , and 4-HNE levels, was observed. Regarding mitochondrial signaling pathways, a significant increase in oxidative capacity (by OCR and OXPHOS levels) was observed. In addition, the PGC-1α, SIRT-1, and PPARδ levels were significantly higher in the LEDT plus idebenone treated-dystrophic muscle cells. Together, the findings suggest that LEDT and idebenone treatment, alone or in conjunction, can modulate the calcium and mitochondrial signaling pathways, such as SLN, SERCA 1, and PGC-1α, contributing towards the improvement of the dystrophic phenotype in mdx muscle cells. In addition, data from the LEDT plus idebenone treatment showed slightly better results than those of each separate treatment in terms of SLN, OXPHOS, and SIRT-1.
(© 2023. The Author(s), under exclusive licence to Cell Stress Society International.)
Databáze: MEDLINE
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