Activation of Nrf2 signaling by Icariin protects against 6 ‐OHDA‐induced neurotoxicity

This study aimed at analyzing whether ICA evoked neuroprotection against 6‐hydroxydopamine (6‐OHDA)‐induced neu rotoxicity in PC12 cells and the mechanisms of action. ICA protected against 6‐OHDA‐induced neuronal damage, accompanied by the inhibition of cell apoptosis through the marked decreases in the Bax/Bcl‐2 ratio, cytochrome C release and caspase‐3 cleavage. In addition, the activation of Nrf2 s ignaling pathway was responsible for ICA‐mediated neuroprotection. First, ICA relieved reactive oxygen species (ROS) accumulation and increased superoxide dismutase (SOD) generation via the activation of Nrf2 signaling. Second, Nrf2 knockdown by siRNA reversed ICA‐mediated neuroprotection. These experiments offer a promising avenue to validate Nrf2 for a compelling target with ICA as a therapeutic strategy to enhance endogenous brain defense mechanisms against Neurodegenerative diseases. (Delete this sentence and change to “Together, these results suggested ICA‐mediated neuroprotection might be attributable to the activation of Nrf2 pathway via anti‐oxidative signaling pathways.”)This article is protected by copyright. All rights reserved
Source: Biotechnology and Applied Biochemistry - Category: Biochemistry Authors: Tags: Original Article Source Type: research