Epigallocatechin gallate protects against TNFα- or H2O2- induced apoptosis. - GreenMedInfo Summary

Oxidative stress, iron dysregulation, and inflammation have been implicated in the pathogenesis of Parkinson's disease (PD). Considering the entwined relationship among these factors, epigallocatechin gallate (EGCG) may be a good candidate for PD treatment due to its protective effects against those factors. The objective of this study is to determine whether EGCG protects N27 dopaminergic neuronal cells from HO- and TNFα- induced neurotoxicity. Seven treatments were included: control, HOTNFα, FeSOHO + EGCGTNFα + EGCG, FeSO + EGCG. Cells were pretreated with 10 μM EGCG, followed by 50 μM HO, 30 ng/ml TNFα or 50 μM FeSO. Neuroprotective effects of EGCG were assessed by cell viability assay, caspase-3 activity, intracellular reactive oxygen species (ROS) generation, and iron related protein expressions. Caspase-3 activity was increased to 2.8 fold (P < 0.001) and 1.5 fold (P < 0.01) with HOand TNFα treatment; However, EGCG pretreatment significantly decreased the caspase activity by 50.2% (P < 0.001) and 30.1% (P < 0.05). Similarly, cell viability was reduced to 69.2% (P < 0.01) and 89% (P < 0.01) by HOand TNFα, which was partially blocked by EGCG pretreatment. Also, EGCG significantly (P < 0.001) protected against HO- induced ROS in a time dependent manner. In addition, both HOand TNFα significantly (P < 0.05) upregulated hepcidin expression and marginally reduced ferroportin (Fpn) expression unlike iron treatment alone. Collectively, our results show that EGCG protects against both TNFα- and HO- induced neuronal apoptosis. The observed neuroprotection may be through the inhibition of oxidative stress and inflammation which is possibly mediated mainly by hepcidin and partially by Fpn.