The protective effect of dopamine against OGD/R injury-induced cell death in HT22 mouse hippocampal cells.

Abstract Previous studies have shown that levo-dopamine ( l -dopa) can improve the consciousness of certain patients with prolonged coma after cerebral ischemia–reperfusion injury, and promote cell growth in vivo. This study aimed to investigate whether l -dopa, which is used clinically to treat Parkinson's disease, might also ameliorate ischemia–reperfusion injury-induced cell death. The oxygen-glucose deprivation and re-oxygenation (OGD/R) model was used to mimic the ischemia–reperfusion pathological process in vitro . HT22 cells were treated with dopamine hydrochloride at different times (i.e., 2 h prior to OGD, during the period of OGD, during the period of R, and throughout the period of OGD/R) and at different concentrations (i.e., 25 μM, 50 μM, 100 μM). Lactate dehydrogenase (LDH) release, flow cytometry–annexin V, and propidium iodide staining with light microscopy showed that dopamine hydrochloride (added during re-oxygenation) promoted cell proliferation and facilitated maintenance of normal cell morphology. However, when present during oxygen-glucose deprivation for 18 h and present throughout OGD/R, dopamine hydrochloride increased cell damage as manifested by shrinkage, rounding up, and reduced viability. In conclusion, dopamine protected HT22 cells from OGD/R injury-induced cell death only at a particular point in time, suggesting that it may be useful for treating severe ischemia–reperfusion brain injury.