Department of Physiology, College of Oriental Medicine, Kyung Hee University, Seoul, Republic of Korea.
Brain Behav Immun. 2012 Nov;26(8):1322-30. doi: 10.1016/j.bbi.2012.08.013. Epub 2012 Sep 5.
In the present study, we sought to determine whether bee venom (BV) promotes the survival of dopaminergic (DA) neurons in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson's disease (PD). Treatment with BV prevented degeneration of DA neurons in the substantia nigra (SN). This neuro-protective effect of BV was associated with microglial deactivation and reduction of CD4 T cell infiltration. Additionally, BV treatment significantly increased the proportion of CD4(+)CD25(+)Foxp3(+) Tregs in vivo and in vitro. The increased proportion of Tregs by BV treatment remained suppressive ex vivo. Interestingly, BV treatment did not prevent MPTP neurotoxicity in mice depleted of Tregs by anti-CD25 antibody injection. Therefore, our present studies suggest that modulation of peripheral immune tolerance by Treg may contribute to the neuroprotective effect of BV in the MPTP model of Parkinson's disease.
在本研究中，我们试图确定蜂毒（BV）是否能促进 1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）诱导的帕金森病（PD）小鼠模型中多巴胺能（DA）神经元的存活。BV 治疗可防止黑质（SN）中 DA 神经元的变性。BV 的这种神经保护作用与小胶质细胞失活和 CD4 T 细胞浸润减少有关。此外，BV 治疗还可显著增加体内和体外 CD4(+)CD25(+)Foxp3(+)Treg 的比例。BV 治疗增加 Treg 的比例在体外仍具有抑制作用。有趣的是，BV 治疗并不能预防用抗 CD25 抗体注射耗尽 Treg 的小鼠的 MPTP 神经毒性。因此，我们的研究表明，Treg 对外周免疫耐受的调节可能有助于 BV 在 MPTP 诱导的帕金森病模型中的神经保护作用。
