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

J Pharmacol Sci. 2019 May;140(1):26-32. doi: 10.1016/j.jphs.2019.03.009. Epub 2019 May 4.

Abstract

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.

Keywords: Anti-inflammatory effects; Melittin; Muscle contusion; Muscle regeneration; Sweet bee venom.

MeSH terms

  • Actins / genetics
  • Actins / metabolism
  • Animals
  • Anti-Inflammatory Agents*
  • 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
  • Mice, Inbred C57BL
  • Muscle, Skeletal / metabolism*
  • MyoD Protein / genetics
  • MyoD Protein / metabolism
  • Myogenin / genetics
  • Myogenin / metabolism
  • Myosin Heavy Chains / genetics
  • Myosin Heavy Chains / metabolism
  • Regeneration / genetics
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Actins
  • Anti-Inflammatory Agents
  • Bee Venoms
  • Ccl2 protein, mouse
  • Chemokine CCL2
  • Inflammation Mediators
  • Interleukin-6
  • MyoD Protein
  • MyoD1 myogenic differentiation protein
  • Myogenin
  • Tumor Necrosis Factor-alpha
  • Melitten
  • Myosin Heavy Chains