在现在的学习,我们在导致的 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP ) 在 dopaminergic 神经原上测试了冷水应力(CWS ) 的效果 Parkinson 是疾病(PD ) 老鼠模型,并且发现那个 CWS 预告的处理得到了更少的 MPTP neurotoxicity。理解位于这现象下面的分子的机制,我们在试验性的鼠标的 striatum 检测了热吃惊蛋白质 70 的表达式(Hsp70 ) ,并且发现那个 CWS 预告的处理能显著地在对待 MPTP 的鼠标增加 striatal Hsp70。与 Hsp70 的正式就职同时,而且, striatal -synuclein 的导致 MPTP 的增加在 CWS +对待 MPTP 的老鼠被禁止。CWS 预告的处理显著地也在 striatum 禁止了 anti-apoptotic 分子 Bcl-2 表示的减小并且在对待 MPTP 的老鼠的 substantia nigra 提高了 Bcl-2 抄写。一起拿,这些数据显示 Hsp70 可能是为对导致 MPTP 的 dopaminergic 毒性的 CWS 的 neuroprotective 效果的重要中介。
In the present study, we tested the effect of cold water stress (CWS) on dopaminergic neurons in 1-methyl- 4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinson's disease (PD) mouse model, and found that CWS pretreatment elicited less MPTP neurotoxicity. To understand the molecular mechanism underlying this phenomenon, we detected the expression of heat shock protein 70 (Hsp70) in the striatum of the experimental mice, and found that CWS pretreatment could significantly increase striatal Hsp70 in MPTP-treated mice. Furthermore, in parallel with the induction of Hsp70, the MPTP-induced increase of striatai α-synuclein was inhibited in the CWS + MPTP-treated mice. CWS pretreatment also significantly inhibited the reduction of anti-apoptotic mol- ecule Bcl-2 expression in the striatum and enhanced Bcl-2 transcription in the substantia nigra of MPTP-treated mice. Taken together, these data indicated that Hsp70 might be an important intermediate for the neuroprotective effect of CWS against MPTP-induced dopaminergic toxicity.