中国神经再生研究(英文版) ›› 2021, Vol. 16 ›› Issue (6): 1005-1010.doi: 10.4103/1673-5374.300447
• 原著:神经损伤修复保护与再生 • 下一篇
恩他卡朋可促进小鼠海马神经发生
Entacapone promotes hippocampal neurogenesis in mice
Dae Young Yoo1, 2, Hyo Young Jung1, Woosuk Kim1, 3, Kyu Ri Hahn1, Hyun Jung Kwon4, Sung Min Nam5, Jin Young Chung6, Yeo Sung Yoon1, Dae Won Kim4, In Koo Hwang1, *
- 1 Department of Anatomy and Cell Biology, College of Veterinary Medicine, and Research Institute for Veterinary Science, Seoul National University, Seoul, South Korea; 2 Department of Anatomy, College of Medicine, Soonchunhyang University, Cheonan, South Korea; 3 Department of Biomedical Sciences, and Research Institute for Bioscience and Biotechnology, Hallym University, Chuncheon, South Korea; 4 Department of Biochemistry and Molecular Biology, Research Institute of Oral Sciences, College of Dentistry, Gangneung-Wonju National University, Gangneung, South Korea; 5 Department of Anatomy, College of Veterinary Medicine, Konkuk University, Seoul, South Korea; 6 Department of Veterinary Internal Medicine and Geriatrics, College of Veterinary Medicine, Kangwon National University, Chuncheon, South Korea
摘要：
儿茶酚-O-甲基转移酶抑制剂恩他卡朋可增强左旋多巴治疗帕金森病的效果,但其是否会影响小鼠海马的神经发生则少见报道。为研究了多巴胺的调节剂恩他卡朋对健康小鼠海马齿状回中细胞增殖和未成熟神经元的影响，实验随机将7周龄雄性小鼠分为溶媒对照组和10，50和200 mg/kg 恩他卡朋干预组。结果发现，50和200 mg/kg恩他卡朋增加了小鼠新物体识别的探索时间。免疫组化染色结果显示，恩他卡朋干预后，小鼠海马齿状回中Ki67阳性增殖细胞和DCX阳性未成熟神经元以及磷酸化cAMP反应元件结合蛋白（pCREB）阳性细胞数量明显增加。Western blot检测结果显示，TrkB受体拮抗剂治疗明显减少了小鼠新物体识别的探索时间，并抑制了海马中磷酸化TrkB和脑源性神经营养因子的表达，而恩他卡朋处理则拮抗了TrkB受体拮抗剂的作用。实验结果表明，恩他卡朋可通过激活BDNF-TrkB-pCREB信号通路以促进海马神经发生和改善记忆功能。实验于2014年2月24日经首尔国立大学动物保护与使用委员会批准（批准号SNU-130730-1）
https://orcid.org/0000-0002-0533-4638 (In Koo Hwang)