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Melittin attenuates neuroinflammatory events in ALS animal model
Author(s) -
Yang Eun Jin,
Kim Seonhwy,
Jiang Jing Hua,
Lee Sang Min,
Choi SunMi
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.441.3
Amyotrophic lateral sclerosis (ALS), paralyzing disorder is characterized by the progressive degeneration and death of motor neurons occurring both as a sporadic and a familial disease. Mutant SOD1(mtSOD1) induces vulnerability of motor neurons through protein misfolding, mitochondrial dysfunction, oxidative damage, cytoskeletal abnormalities and defective axonal transport, excitotoxicity, inadequate growth factor signaling, and neuro inflammation. Melittin consisting of 26 amino acid residue is one of components of bee venom known as an Oriental medicine and has been reported the evidence in the literature, inhibition of cancer cell proliferation, anti‐inflammatory and anti‐arthritic effects. The purpose of the present study is to determine whether melittin is able to suppress the motor neuron loss and microglial cell action in hG93ASOD1 mouse commonly used model for inherited ALS. Meltittin was treated at the ‘ZuSanLi’ (ST36) acupuncture point in hSODG93A animal model. Melittin treated animals showed the decrease of the number of microglia and the expression level of phospho‐p38 in spinal cord and brain stem in mutant hSOD1 transgenic mice. Interestingly, melittin treatment in symptomatic ALS animals improved motor activity and reduced the neuronal cell death in spinal cord compared to the control group. Our research suggests a potential functional link between metlittin and anti‐neuroinflammation in ALS animal model.