title: 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.
authors: Institute of Rehabilitation Medicine of China, Chinese Institute of Rehabilitation Science, China Rehabilitation Research Center, Beijing, PR China; Beijing Key Laboratory of Neural Injury and Rehabilitation, PR China.
authors: Wenzhu
authors: W
authors: Wang
authors: Institute of Rehabilitation Medicine of China, Chinese Institute of Rehabilitation Science, China Rehabilitation Research Center, Beijing, PR China; Beijing Key Laboratory of Neural Injury and Rehabilitation, PR China.
authors: Lixi
authors: L
authors: Zhao
authors: Institute of Rehabilitation Medicine of China, Chinese Institute of Rehabilitation Science, China Rehabilitation Research Center, Beijing, PR China; Beijing Key Laboratory of Neural Injury and Rehabilitation, PR China.
authors: Fan
authors: F
authors: Bai
authors: Beijing Bo Ai Hospital, China Rehabilitation Research Center, Beijing, PR China; School of Rehabilitation Medicine, Capital Medical University, Beijing, PR China.
authors: Tong
authors: T
authors: Zhang
authors: Beijing Bo Ai Hospital, China Rehabilitation Research Center, Beijing, PR China; Institute of Rehabilitation Medicine of China, Chinese Institute of Rehabilitation Science, China Rehabilitation Research Center, Beijing, PR China.
authors: Hao
authors: H
authors: Dong
authors: Beijing Bo Ai Hospital, China Rehabilitation Research Center, Beijing, PR China; School of Rehabilitation Medicine, Capital Medical University, Beijing, PR China. Electronic address: liulixu_crrc@163.com.
authors: Lixu
authors: L
authors: Liu
mesh_terms: D000818:Animals; D016923:Cell Death; D002460:Cell Line; D004298:Dopamine / Q000494:pharmacology*; D005947:Glucose; D006624:Hippocampus; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D051379:Mice; D010100:Oxygen; D020011:Protective Agents / Q000494:pharmacology*
chemical_list: D020011:Protective Agents; D007770:L-Lactate Dehydrogenase; D005947:Glucose; D010100:Oxygen; D004298:Dopamine
keywords: Cerebral ischemia–reperfusion injury; Dopamine; HT22 cells; The oxygen-glucose deprivation and re-oxygenation (OGD/R) injury