Abstract
The aim of the present study was to examine the effects of butorphanol on neural injury in an oxygen glucose deprivation/reoxygenation (OGD/R) model using PC12 cells, and to investigate whether mitochondrial apoptosis was involved in these effects. To establish the OGD/R model, PC12 cells were cultured under hypoxia and low glucose conditions. Expression levels of inflammatory cytokines were evaluated by detecting the levels of tumor necrosis factor‑α, interleukin (IL)‑1β, IL‑6 and monocyte chemoattractant protein‑1. Oxidative stress was evaluated by measuring the levels of reactive oxygen species, lactate dehydrogenase activity and myeloperoxidase concentration. Apoptosis, protein expression and cell viability were determined by flow cytometry, western blotting and by using a Cell Counting Kit‑8, respectively. Compared with the control group, cell viability, expression of inflammatory factors and oxidative stress were all decreased in the OGD/R group. All the above changes could be mitigated by treatment with butorphanol. In addition, butorphanol treatment resulted in a significant upregulation of Bax, and downregulation of Bcl‑2, activated caspase‑3, caspase‑9 and poly ADP‑ribose polymerase, increased the expression of X‑linked inhibitor of apoptosis protein and enhanced ATP activity. To conclude, these results suggested that the protective effects of butorphanol are associated with the inhibition of OGD/R‑induced inflammation and apoptosis injury, and may be partially associated with the inhibition of mitochondrial apoptosis.