Melittin ameliorates the inflammation of organs in an
amyotrophic lateral sclerosis animal model
Exp Neurobiol, 2014 Mar;23(1):86-92
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.
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