Cryptotanshinone protects hippocampal neurons against oxygen-glucose deprivation-induced injury through the activation of Nrf2/HO-1 signaling pathway

Cryptotanshinone (CPT), a terpenoid isolated from the roots of Salvia miltiorrhiza Bunge, was reported to have neuroprotective effects against cerebral ischemic stroke. However, the exact molecular mechanism underlying its neuroprotective ability remains unclear. The present study aimed to explore the regulatory effects of CPT on oxygen-glucose deprivation/reoxygenation (OGD/R)-induced cell injury in a model of hippocampal neurons. Our results demonstrated that CPT improved cell viability and reduced the lactate dehydrogenase leakage in OGD/R-stimulated hippocampal neurons. In addition, CPT significantly inhibited oxidative stress and apoptosis in hippocampal neurons after OGD/R stimulation. Furthermore, CPT significantly enhanced the nuclear translocation of the nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) expression in hippocampal neurons exposed to OGD/R. Moreover, Nrf2 knockdown reversed the anti- apoptotic and anti-oxidant activities of CPT in primary hippocampal neurons exposed to OGD/R. In conclusion, these findings demonstrated that CPT attenuated oxidative stress and neuronal apoptosis after OGD/R injury through the activation of Nrf2/HO-1 signaling pathway in hippocampal neurons. Thus, CPT may be a novel therapeutic agent for cerebral I/R injury.

Automated summary

CPT attenuates oxidative stress and neuronal apoptosis in hippocampal neurons after OGD/R injury by activating the Nrf2/HO-1 signaling pathway, suggesting that it could be a novel therapeutic agent for cerebral ischemia/reperfusion injury.