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Updated: May 1, 2026
Preparation and Culture of Myogenic Precursor Cells/Primary Myoblasts from Skeletal Muscle of Adult and Aged Humans
Published on: February 16, 2017
Muscle homing peptide modified liposomes loaded with EGCG improved skeletal muscle dysfunction by inhibiting
Zongyu Huang1, Jianjie Xie1, Nana Gao2
1Department of Endocrinology, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning 121001, China.
Abstract:
Skeletal muscle aging frequently leads to a reduction in muscle mass and strength, significantly compromising the quality of life in elderly individuals. Skeletal muscle dysfunction during aging is widely recognized to be closely linked to chronic inflammation, oxidative stress and mitochondrial dysfunction. In this study, we confirmed the successful synthesis of M12 (muscle homing peptide)-modified EGCG (Epigallocatechin gallate) liposomes and validated their specific targeting to skeletal muscle through immunofluorescence analysis and in vivo imaging in small animal models. Both in vivo and in vitro experiments demonstrated that M12EGLP effectively suppressed the expression of inflammatory markers such as TNF-α and IL-6, thereby alleviating oxidative stress and restoring mitochondrial function in skeletal muscle. These effects ultimately contributed to the improvement of skeletal muscle dysfunction in aging mice. We have developed M12-modified EGCG liposomes (M12EGLP), a targeted drug delivery system capable of specifically accumulating in skeletal muscle, thereby enhancing the bioavailability and therapeutic potential of EGCG. M12EGLP enhances the exercise capacity of aging mice by reducing skeletal muscle inflammation, which subsequently alleviates oxidative stress and improves mitochondrial function. Therefore, as a novel and targeted drug delivery system, M12EGLP may provide a promising therapeutic strategy for the clinical management of age-related skeletal muscle dysfunction.
Insights
Researchers developed M12-modified Epigallocatechin gallate (EGCG) liposomes (M12EGLP) to target aging skeletal muscles. This novel drug delivery system reduces inflammation, oxidative stress, and improves mitochondrial function, enhancing muscle health in aging mice.
Area of Science:
- Gerontology
- Pharmacology
- Biomedical Engineering
Background:
- Skeletal muscle aging is characterized by reduced mass and strength, impacting elderly quality of life.
- Age-related muscle dysfunction is linked to chronic inflammation, oxidative stress, and mitochondrial dysfunction.
- Epigallocatechin gallate (EGCG) shows potential therapeutic benefits but lacks targeted delivery.
Purpose of the Study:
- To develop and validate M12-modified EGCG liposomes (M12EGLP) as a targeted drug delivery system for skeletal muscle.
- To investigate the efficacy of M12EGLP in ameliorating age-related skeletal muscle dysfunction in mice.
- To assess the impact of M12EGLP on inflammatory markers, oxidative stress, and mitochondrial function in aging muscle.
Main Methods:
- Synthesis of M12 (muscle homing peptide)-modified EGCG liposomes (M12EGLP).
- Validation of skeletal muscle targeting using immunofluorescence and in vivo imaging in small animal models.
- In vivo and in vitro experiments to evaluate the suppression of inflammatory markers (TNF-α, IL-6), alleviation of oxidative stress, and restoration of mitochondrial function.
Main Results:
- M12EGLP demonstrated specific targeting to skeletal muscle.
- M12EGLP effectively suppressed inflammatory markers like TNF-α and IL-6 in aging skeletal muscle.
- Treatment with M12EGLP alleviated oxidative stress, restored mitochondrial function, and improved skeletal muscle dysfunction in aging mice.
- M12EGLP enhanced exercise capacity in aging mice.
Conclusions:
- M12EGLP is a novel, targeted drug delivery system that specifically accumulates in skeletal muscle.
- M12EGLP enhances EGCG bioavailability and therapeutic potential for age-related muscle dysfunction.
- M12EGLP offers a promising therapeutic strategy for managing age-related skeletal muscle decline by reducing inflammation and oxidative stress.
