Melittin Ameliorates the Inflammation of Organs in an Amyotrophic Lateral Sclerosis Animal Model.
- Author:
Sun Hwa LEE
1
;
Sun Mi CHOI
;
Eun Jin YANG
Author Information
- Publication Type:Original Article
- Keywords: Amyotrophic lateral sclerosis (ALS); hSOD1(G93A); Melittin; inflammation
- MeSH: Amyotrophic Lateral Sclerosis*; Animals*; Bee Venoms; Brain Stem; Cause of Death; Cell Survival; Extremities; Immune System; Inflammation*; Liver; Lung; Melitten*; Mice; Mice, Transgenic; Models, Animal*; Motor Cortex; Motor Neurons; Muscles; Neurodegenerative Diseases; Spinal Cord; Spleen
- From:Experimental Neurobiology 2014;23(1):86-92
- CountryRepublic of Korea
- Language:English
- Abstract: 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.
