Triptolide attenuated injury via inhibiting oxidative stress in Amyloid-Beta(25-35)-treated differentiated PC12 cells

摘要

Background: Recently, an abnormal deposition of Amyloid-Beta (A beta) was considered the primary cause of the pathogenesis of Alzheimer's disease (AD). And how to inhibit the cytotoxicity is considered an important target for the treatment of AD. Triptolide (TP), a purified diterpenoid from the herb Tripterygium wilfordii Hook. f. (TWHF), has potential neuroprotective effects pertinent to disease of the nervous system. However, whether triptolide and its specific mechanisms have protective functions in differentiated PC12 cells treated with A beta(25-35) remain unclear.