1. Neuroprotective effects of bee venom phospholipase A2 in the 3xTg AD mouse model of Alzheimer’s disease
- Author
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Insop Shim, Chanju Lee, Minsook Ye, Moon Sik Yoon, Deok-Sang Hwang, A. Ram Yu, Hyunsu Bae, Jin Su Kim, and Hwan-Suck Chung
- Subjects
0301 basic medicine ,Pharmacology ,Hippocampus ,T-Lymphocytes, Regulatory ,Amyloid beta-Protein Precursor ,Mice ,0302 clinical medicine ,Alzheimer's disease ,Regulatory T cells ,Bee venom phospholipase A2 ,Microglia ,Neuroinflammation ,PET ,Escape Reaction ,education.field_of_study ,biology ,Learning Disabilities ,General Neuroscience ,FOXP3 ,Bee Venoms ,medicine.anatomical_structure ,Neuroprotective Agents ,Neurology ,Cell activation ,Alzheimer’s disease ,Amyloid beta ,Population ,Immunology ,Mice, Transgenic ,tau Proteins ,Neuroprotection ,03 medical and health sciences ,Cellular and Molecular Neuroscience ,Phospholipase A2 ,Alzheimer Disease ,Antigens, CD ,Fluorodeoxyglucose F18 ,medicine ,Presenilin-1 ,Animals ,Humans ,education ,Maze Learning ,Radionuclide Imaging ,Research ,Body Weight ,Disease Models, Animal ,Phospholipases A2 ,030104 developmental biology ,Mutation ,biology.protein ,030217 neurology & neurosurgery - Abstract
Background: Alzheimer's disease (AD) is a severe neuroinflammatory disease. CD4(+) Foxp3(+) regulatory T cells (Tregs) modulate various inflammatory diseases via suppressing Th cell activation. There are increasing evidences that Tregs have beneficial roles in neurodegenerative diseases. Previously, we found the population of Treg cells was significantly increased by bee venom phospholipase A2 (bvPLA2) treatment in vivo and in vitro. Methods: To examine the effects of bvPLA2 on AD, bvPLA2 was administered to 3xTg-AD mice, mouse model of Alzheimer's disease. The levels of amyloid beta (A beta) deposits in the hippocampus, glucose metabolism in the brain, microglia activation, and CD4(+) T cell infiltration were analyzed to evaluate the neuroprotective effect of bvPLA2. Results: bvPLA2 treatment significantly enhanced the cognitive function of the 3xTg-AD mice and increased glucose metabolism, as assessed with 18F-2 fluoro-2-deoxy-D-glucose ([F-18] FDG) positron emission tomography (PET). The levels of A beta deposits in the hippocampus were dramatically decreased by bvPLA2 treatment. This neuroprotective effect of bvPLA2 was associated with microglial deactivation and reduction in CD4(+) T cell infiltration. Interestingly, the neuroprotective effects of bvPLA2 were abolished in Treg-depleted mice. Conclusions: The present studies strongly suggest that the increase of Treg population by bvPLA2 treatment might inhibit progression of AD in the 3xTg AD mice.
- Published
- 2016