Abstract
Abstract In the present study, we examined whether bee venom (BV) promotes the survival of nigrostriatal dopaminergic (DA) neurons in the MPTP-induced Parkinson’s disease (PD) mice model. Treatment of BV prevented degeneration of nigrostriatal DA neurons, increased striatal dopamine levels, and improved motor function. This nueroprotection afforded by bee venom was associated with the suppression of microglia and inhibition of recruitment of CD4+ T cells. Additionally, CD4+CD25+Foxp3+ Treg cells were significantly increased in vivo and in vitro after treatment of BV. Therefore, we carefully propose that neuroprotection of BV might be associated with its anti-inflammatory properties and could be employed as novel therapeutic agents for PD and other disorders associated with neuroinflammation.
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