摘要

Nuclear factor erythroid 2-related factor 2 (Nrf2) coordinates the up-regulation of cytoprotective genes via the antioxidant response element (ARE). There is significant evidence that oxidative stress is a critical event in the pathogenesis of AD. Considering the protective role of Nrf2 against oxidative injury, we studied to determine whether in vivo toxicity of amyloid beta (A beta) can be attenuated by tBHQ, an Nrf2 stabilizer, Using an A beta injection model. We demonstrated that pre-activation of endogenous Nrf2 by tBHQ attenuated A beta-induced caspase-3 expression. tBHQ enhanced GSH, decreased MDA level, and inhibited NF-kappa B. This investigation provides the first documentation of tBHQ's neuroprotective effect through decrease of A beta accumulation in rat brain. Our results show the involvement of Hsp-70 in this protective effect. In summary tBHQ treatment for 1 week prior to A beta injection protected against the oxidative damage, apoptosis and A beta accumulation in rats.

  • 出版日期2011-5