Melittin – A bee venom component – Enhances muscle regeneration factors expression in a mouse model of skeletal muscle contusion

• Published in: Journal of pharmacological sciences Vol. 140; no. 1; pp. 26 - 32
• Main Authors: Lee, Jae Eun, Shah, Vikash Kumar, Lee, Eun-Jung, Oh, Min-Seok, Choi, Jeong June
• Format: Journal Article
• Language: English
• Published: Japan Elsevier B.V 01.05.2019; Elsevier
• Subjects: Actins - genetics; Actins - metabolism; Animals; Anti-Inflammatory Agents; Anti-inflammatory effects; Bee Venoms - pharmacology; Bee Venoms - therapeutic use; Chemokine CCL2 - metabolism; Contusions - drug therapy; Contusions - genetics; Contusions - metabolism; Disease Models, Animal; Dose-Response Relationship, Drug; Gene Expression; Inflammation Mediators - metabolism; Interleukin-6 - metabolism; Male; Melitten - pharmacology; Melitten - therapeutic use; Melittin; Mice, Inbred C57BL; Muscle contusion; Muscle regeneration; Muscle, Skeletal - metabolism; MyoD Protein - genetics; MyoD Protein - metabolism; Myogenin - genetics; Myogenin - metabolism; Myosin Heavy Chains - genetics; Myosin Heavy Chains - metabolism; Regeneration - genetics; Sweet bee venom; Tumor Necrosis Factor-alpha - metabolism; Melittin; Sweet bee venom; Anti-inflammatory effects; Muscle regeneration; Muscle contusion
• ISSN: 1347-8613; 1347-8648
• DOI: 10.1016/j.jphs.2019.03.009

Melittin is a major peptide component of sweet bee venom that possesses anti-allergic, anti-inflammatory, anti-arthritis, anti-cancer, and neuroprotective properties. However, the therapeutic effects of melittin on muscle injury have not been elucidated. We investigated the therapeutic effects of melittin on muscle injury in a mouse model of muscle contusion. The biceps femoris muscle of the mice was injured using drop mass method, and the animals were treated with melittin (4, 20, or 100 μg/kg) for 7 days. Melittin significantly increased: locomotor activity in open field test, and treadmill running activity in a dose-dependent manner to level comparable to the positive control, diclofenac (30 mg/kg). Melittin treatment attenuated the pro-inflammatory cytokine MCP-1, TNF-α and IL-6. The expression of muscle regeneration biomarkers, including MyoD (muscle differentiation marker), myogenin, smooth muscle actin, and myosin heavy chain was markedly increased in the injured muscle tissue of melittin-treated mice, as determined by western blotting and quantitative real-time polymerase chain reaction. These results demonstrate that melittin inhibits inflammatory response and improves muscle damage by regenerating muscles in a mouse model of muscle contusion. Taken together, the results of present study suggest that melittin is a promising candidate for the muscle injury treatment.