低水平光生物调节疗法调节营养不良肌肉中H2O2生成、TRPC-6和PGC-1α水平。

Caroline Covatti, Daniela Sayuri Mizobuti, Guilherme Luiz da Rocha, Heloina Nathalliê Mariano da Silva, Caroline Caramano de Lourenço, Adriana Pertille, Elaine Cristina Leite Pereira, Elaine Minatel
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引用次数: 1

摘要

目的:本研究评估光生物调节疗法(PBMT)对Duchenne肌营养不良(DMD) mdx小鼠(肌细胞)和体内(腓骨肌)线粒体生物发生相关因子、线粒体呼吸复合物以及瞬时受体电位规范通道(如TRPC-1和TRPC-6)的影响。背景:目前还没有成功的治疗DMD的方法,因此需要寻找新的治疗方法来改善肌肉的功能、生活质量和营养不良患者的生存。方法:营养不良原代肌细胞分别在0.6 J和5j时接受PBMT,营养不良腓肠肌在0.6 J时接受PBMT。结果:PBMT (0.6 J和5 J)处理后的肌营养不良细胞无细胞毒性,过氧化氢(H2O2)生成水平显著降低。我们还首次证明,在低剂量(0.6 J)下,PBMT能够降低营养不良腓肠肌中TRPC-6的含量,并提高过氧化物酶体增殖体激活受体γ共激活因子-1α (PGC-1α)的含量。结论:PBMT调节营养不良肌肉中H2O2的产生、TRPC-6和PGC-1α的含量。提示激光治疗可作为营养不良患者的辅助治疗方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Low-Level Photobiomodulation Therapy Modulates H2O2 Production, TRPC-6, and PGC-1α Levels in the Dystrophic Muscle.

Objective: This study evaluated photobiomodulation therapy (PBMT) effects on the factors involved in mitochondrial biogenesis, on the mitochondrial respiratory complexes, and on the transient receptor potential canonical channels (such as TRPC-1 and TRPC-6) in in vitro (mdx muscle cells) and in vivo studies (gastrocnemius muscle) from mdx mice, the dystrophin-deficient model of Duchenne muscular dystrophy (DMD). Background: There is no successful treatment for DMD, therefore demanding search for new therapies that can improve the muscle role, the quality of life, and the survival of dystrophic patients. Methods: The dystrophic primary muscle cells received PBMT at 0.6 J and 5 J, and the dystrophic gastrocnemius muscle received PBMT at 0.6 J. Results: The dystrophic muscle cells treated with PBMT (0.6 J and 5 J) showed no cytotoxicity and significantly lower levels in hydrogen peroxide (H2O2) production. We also demonstrated, for the first time, the capacity of PBMT, at a low dose (0.6 J), in reducing the TRPC-6 content and in raising the peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) content in the dystrophic gastrocnemius muscle. Conclusions: PBMT modulates H2O2 production, TRPC-6, and PGC-1α content in the dystrophic muscle. These results suggest that laser therapy could act as an auxiliary therapy in the treatment of dystrophic patients.

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