Evidence indicates that extracellular auto-oxidation, which occurs through the generation of toxic products, such as hydrogen peroxide, oxygen-derived radicals, semiquinones, and quinones, plays an important role in 6-OHDA-induced cytotoxicity. The consumption of flavonoid rich foods and beverages has been suggested to limit the neurodegeneration associated with a variety of neurological disorders, and to prevent or reverse normal or abnormal deteriorations in cognitive performance. Luteolin, a flavone ubiquitously distributed in several types of vegetables, fruits, and medicinal herbs, has antioxidant activity by directly scavenging ROS. Luteolin also inhibits 6-OHDA-induced apoptosis and depresses the 6-OHDA-enhanced Bax/Bcl-2 ratio and p53 expression in PC12 cells. In addition to cytoprotective effects, we have reported that luteolin is a neurotrophic agent, and its action is in part through up-regulation of miR-132, thereby activating the cAMP/PKA- and ERK-dependent CREB signaling pathways in PC12 cells. However, little information is available about how luteolin affects Decoquinate transcriptional change of cellular stress response pathways in response to 6-OHDA in PC12 cells. The results first confirmed that 6-OHDA induced ROS overproduction, caspase-3 activation and cell death. Three different types of antioxidants, namely luteolin, tiron, and lipoic acid, were then used to test their cytoprotective potencies. It has been shown that luteolin can directly CGP 57380 quench all kinds of ROS, including superoxide, hydrogen peroxide, singlet oxygen and hydroxyl radical in vitro. Luteolin also regulates a variety of cell signaling pathways leading to its high neuroprotective efficacy. In addition to being a cellular permeable superoxide scavenger, tiron inhibits the phosphorylation of ROS-induced JNK, which plays a key role in 6-OHDA-induced cell death in PC12 cells. LA acts against free radicals, increases or maintains cellular GSH levels, regulates the redox state in the cells, and affects gene expression. Both luteolin and tiron can block 6-OHDA-mediated ROS production, as detected by reduced DCF fluorescence, and thus significantly restore cell viability.