The role that inflammation plays in skeletal muscle is not quite clear as it looks. Inflammatory mediators behave in a dual fashion in muscle cells. During injury, cytokines and chemokines stimulate muscle repair and regeneration via activation of myoblasts, a core event in muscle remodeling [108]. Similarly, serum and muscle levels of IL-6 temporarily increase following physical exercise, and IL-6 blocks the activity of catabolic cytokines such as TNF-α. On the other hand, chronic inflammation in muscle cells, which correlates with persistent mitochondrial dysfunction and metabolic dysregulation, pathologically activates muscle fiber transformation and atrophy, eventually resulting in the development of sarcopenia [23,114]. It seems that bee products also act dually in skeletal muscle: they support the activity of cytokines that promote muscle remodeling [108] and suppress muscle-consuming cytokines [38,101,108]. In this regard, treating undifferentiated C2C12 myoblasts with ethanolic extracts of Brazilian propolis (100 μg/mL for 8 h) triggered the migration of RAW264 macrophage and increased their production of angiogenic factors (e.g., vascular endothelial growth factor A (VEGF-A) and metalloproteinase-12 (MMP-12)), chemokines (e.g., CCL-2 and CCL-5), and cytokines (e.g., IL-6, which increased by 40-folds). Propolis inhibited the expression of IL-1β and TNF-α at 4, 8, and 12 h of incubation. These effects were nuclear factor kappa B (NF-κB)-dependent given that propolis simultaneously increased nuclear translocation of p65 and p50 NF-κB proteins 3 h after treatment. Meanwhile, inhibiting IκB kinase (IKK) by BMS-345541 profoundly hindered the effect of propolis on the expression of CCL-2, CCL-5, and IL-6 by 66%, 81%, and 69%, respectively. Propolis also enhanced the expression of MAIL/IκBζ. This molecule modulates chromatin and selectively induces the production of IL-6, leukemia inhibitory factor (LIF), and CCL-2 [108].