(-)-Epicatechin accelerates muscle repair and promotes hypertrophy in type 2 fibers of BaCl2-damaged gastrocnemius in CD1 mice.

Skeletal muscle exhibits remarkable plasticity, allowing it to adapt to varying metabolic and regenerative demands. However, conditions such as myopathies compromise its integrity. To study muscle degeneration and regeneration, various models have been developed, including chemical injury induced by BaCl₂. This agent causes myofiber damage similar to that produced by certain biological toxins, yet it spares satellite cells, thereby enabling regeneration. Key regulators such as MyoD and active β-catenin are essential for activating myogenic pathways during repair, although their behavior may vary across muscle types. Currently, there is limited information on effective treatments for many myopathies. Epicatechin (Epi), a natural flavonoid, has shown potential to reduce fibrosis and promote myogenic protein expression. In this study, we evaluated the effect of Epi on gastrocnemius muscle repair following BaCl₂-induced injury in CD1 mice. A total of 60 mice were divided into four groups (n = 3 for morphology and gene expression analysis, and n = 6 for western blot analysis). The results showed that Epi reduced the injury area compared to the untreated groups. Active β-catenin and MyoD levels increased within 1 h post-injury, while Myogenin expression continued to rise up to 24 h. Interestingly, the non-injured plus Epi group also showed increased levels of MyoD and Myogenin, as well as increased cross-sectional area (CSA). Additionally, Epi appeared to influence the expression of myosin heavy-chain isoforms and to induce differential hypertrophy in type II muscle fibers, findings warranting further investigation. Moreover, (-)-Epicatechin accelerated muscle repair and reduced muscle injury, suggesting its potential as a supportive agent in muscle repair therapies.