Protective effect of catalpol on oxygen glucose deprivation neurons

Brain ischemia is one common cerebrovascular disease with unfavorable prognosis and higher morbidity and mortality rates. The re-perfusion injury after primary ischemia further aggravated the progression of cerebral ischemia. The development of effective drugs for protecting neurons during brain ischemia-reperfusion damage is thus of critical importance. With pluripotent bioactivities, the protective role of catalpol on oxygen glucose deprivation (OGD) neurons was studied. PC12 cells were prepared for OGD model, followed by the treatment using gradient concentrations of catalpol (0.1 mM, 1 mM and 2 mM). Cell proliferation was detected by MTT assay. The activity of lactate dehydrogenase (LDH), superoxide dismutase (SOD) and reactive oxygen species (ROS) was further tested. The level of caspase-3, tumor necrosis factor α (TNF-α), and interleukin-1β (IL-1β) was tested by enzyme linked immunosorbent assay (ELISA). Compared to control group, the survival of OGD model cells was decreased, accompanied with higher LDH and ROS levels and lower SOD level. The expression of inflammatory cytokine TNF-α and IL-1β were potentiated. Catalpol was found to facilitate cell survival, lower LDH, ROS, caspase-3, TNF-α and IL-1β expression while increase SOD activity (P<0.05) in a dose-dependent manner. Catalpol can inhibit apoptosis and inflammation via modulating oxidation homeostasis, and protect OGD injury neurons.