Amyotrophic lateral sclerosis (ALS) is a devastating progressive
neurodegenerative disorder characterized by a selective loss of motor neurons in the spinal cord, brainstem, and motor cortex, leading to weakness of the limb and bulbar muscles. Although the immediate cause of death in ALS is the destruction of motor neurons, ALS is a multi-organ disease that also affects the lungs, spleen, and liver.
Melittin is one of components of
bee venom and has anti-neuroinflammatory effects in the spinal cord, as shown in an ALS animal model. To investigate the effects of
melittin on
inflammation in the lungs and spleen, we used hSOD1(G93A) transgenic mice that are mimic for ALS.
Melittin treatment reduced the expression of inflammatory
proteins, including Iba-1 and CD14 by 1.9- and 1.3-fold (p<0.05), respectively, in the lungs of symptomatic hSOD1(G93A) transgenic mice. In the spleen, the expression of CD14 and COX2 that are related to
inflammation were decreased by 1.4 fold (p<0.05) and cell survival
proteins such as pERK and Bcl2 were increased by 1.3- and 1.5-fold (p<0.05) in the
melittin-treated hSOD1G93A transgenic mice. These findings suggest that
melittin could be a candidate to regulate the immune system in organs affected by ALS.