Bee venom phospholipase A2 ameliorates motor dysfunction and modulates microglia activation in Parkinson’s disease alpha-synuclein transgenic mice

Abstract

α-Synuclein (α-Syn) has a critical role in microglia-mediated neuroinflammation, which leads to the development of Parkinson’s disease (PD). Recent studies have shown that bee venom (BV) has beneficial effects on PD symptoms in human patients or 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) toxin-induced PD mice. This study investigated whether treatment with BV-derived phospholipase A2 (bvPLA2) would improve the motor dysfunction and pathological features of PD in human A53T α-Syn mutant transgenic (A53T Tg) mice. The motor dysfunction of A53T Tg mice was assessed using the pole test. The levels of α-Syn, microglia and the M1/M2 phenotype in the spinal cord were evaluated by immunofluorescence. bvPLA2 treatment significantly ameliorated motor dysfunction in A53T Tg mice. In addition, bvPLA2 significantly reduced the expression of α-Syn, the activation and numbers of microglia, and the ratio of M1/M2 in A53T Tg mice. These results suggest that bvPLA2 could be a promising treatment option for PD. An enzyme in bee venom ameliorates symptoms of Parkinson's disease in mice, providing a key to understanding a disease afflicting millions. A Korean team led by Hyunsu Bae from Kyung Hee University in Seoul investigated the activity of the bee-venom-derived phospholipase A2 (PLA2), which alters a brain pathway linked to Parkinson's disease. In a mouse model of Parkinson's disease, they found that repeated infusions of PLA2 improved motor performance in treated mice, compared with untreated mice. In treated mice, immune cell function in the brain switched from an inflammatory ‘cleanup’ mode to a mode associated with repair and regeneration. Elucidating how PLA2 in bee venom alters the progression of Parkinson's disease may provide a potential therapy, while also building our understanding of the causes of this debilitating disease.