Marine Biochemistry Laboratory, Department of Chemistry, Pukyong National University, Busan 608-737, Republic of Korea.
Food Chem. 2013 Nov 15;141(2):1147-57. doi: 10.1016/j.foodchem.2013.04.004. Epub 2013 Apr 13.
Experimental evidence suggests that tyrosol [2-(4-hydroxyphenyl)ethanol] exhibits potent protective activities against several pathogeneses. In this study, we evaluated the protective effect of tyrosol against 1-methyl-4-phenylpyridinium (MPP(+))-induced CATH.a neuron cell death. Tyrosol dose-dependently protected CATH.a cells from MPP(+)-induced cell death and the protection was more apparent after prolong incubation (48h). The data showed that tyrosol treatment suppressed the reduction of phospho-tyrosine hydroxylase level in CATH.a cells. Further, the compound repressed MPP(+)-induced depletion of mitochondrial membrane potential (Δψm) and thereby maintained intracellular ATP production in the cell. The cellular signalling pathway studies revealed that tyrosol protected CATH.a cells from MPP(+)-induced apoptotic signalling, most likely via activation of PI3K/Akt signalling pathway along with up-regulation of anti-oxidative enzymes (SOD-1 and SOD-2) and DJ-1 protein in the cell. Collectively, present study demonstrates that tyrosol significantly protects dopaminergic neurons from MPP(+)-induced degradation, and reveals potential neuroprotective mechanism of tyrosol.
实验证据表明，酪醇[2-(4-羟苯基)乙醇]对多种发病机制表现出强大的保护活性。在这项研究中，我们评估了酪醇对 1-甲基-4-苯基吡啶鎓（MPP(+））诱导的 CATH.a 神经元细胞死亡的保护作用。酪醇呈剂量依赖性保护 CATH.a 细胞免受 MPP(+）诱导的细胞死亡，并且在延长孵育（48 小时）后保护作用更加明显。数据显示，酪醇处理抑制了 CATH.a 细胞中磷酸酪氨酸羟化酶水平的降低。此外，该化合物抑制 MPP(+）诱导的线粒体膜电位（Δψm）耗竭，从而维持细胞内 ATP 的产生。细胞信号通路研究表明，酪醇通过激活 PI3K/Akt 信号通路以及上调细胞内抗氧化酶（SOD-1 和 SOD-2）和 DJ-1 蛋白，从而保护 CATH.a 细胞免受 MPP(+）诱导的凋亡信号。综上所述，本研究表明酪醇可显著保护多巴胺能神经元免受 MPP(+）诱导的降解，并揭示了酪醇的潜在神经保护机制。
