CAJ | 학술논문

目的：通过体外实验观察美金刚对异氟烷所致神经干细胞增殖能力减退的保护作用及其可能机制。方法从出生1 d 的大鼠海马获取神经干细胞,体外培养并随机分为5组：对照组(control 组)、溶剂对照组(Vehicle 组)、异氟烷组(Iso 组)、异氟烷＋美金刚组(Iso＋ Mem 组)和异氟烷＋美金刚＋LY294002组(Iso＋Mem＋LY 组)。通过检测 BrdU 在增殖神经干细胞中的表达了解神经干细胞增殖水平,Western blot 法检测神经元磷酸化 Akt 蛋白表达水平。结果2.4％异氟烷暴露6 h 后神经干细胞增殖能力和磷酸化 Akt 蛋白表达水平均显著下降(P<0.01)。美金刚可同时缓解异氟烷所致神经干细胞增殖能力减退和磷酸化 Akt 蛋白表达水平下降(P<0.01)。 Akt 通路特异性抑制剂 LY294002可逆转美金刚对神经干细胞增殖的保护作用(P<0.01)。结论美金刚可通过激活 Akt 信号转导通路,缓解异氟烷所致神经干细胞增殖能力减退。
목적：통과체외실험관찰미금강대이불완소치신경간세포증식능력감퇴적보호작용급기가능궤제。방법종출생1 d 적대서해마획취신경간세포,체외배양병수궤분위5조：대조조(control 조)、용제대조조(Vehicle 조)、이불완조(Iso 조)、이불완＋미금강조(Iso＋ Mem 조)화이불완＋미금강＋LY294002조(Iso＋Mem＋LY 조)。통과검측 BrdU 재증식신경간세포중적표체료해신경간세포증식수평,Western blot 법검측신경원린산화 Akt 단백표체수평。결과2.4％이불완폭로6 h 후신경간세포증식능력화린산화 Akt 단백표체수평균현저하강(P<0.01)。미금강가동시완해이불완소치신경간세포증식능력감퇴화린산화 Akt 단백표체수평하강(P<0.01)。 Akt 통로특이성억제제 LY294002가역전미금강대신경간세포증식적보호작용(P<0.01)。결론미금강가통과격활 Akt 신호전도통로,완해이불완소치신경간세포증식능력감퇴。
Objective To investigate the protective effects of memantine on isofluane￣induced decrease of proliferation in neural stem cells ( NSCs) and the potential mechanisms in vitro. Methods Neural stem cells were isolated from rat hippocampi (postnatal day 1) and grew in culture. Cultured NSCs were randomly divided into the control ( Group Control), Vehicle (Group Vehicle), Isoflurane ( Group Iso), Isoflurane +Memantine ( Group Iso +Mem) and Isoflurane + Memantine +LY294002 groups (Group Iso+Mem+LY).Proliferation was assessed by cell counting and BrdU incorporation.Western blot was conducted to detect protein expression of phospho￣Akt. Results Compared with the control group,BrdU incorporation and phospho￣Akt expressions in neural stem cells significantly declined after 2.4% isoflurane exposure for 6 h (P<0.01).However, isofluane￣induced decrease of BrdU incorporation and phospho￣Akt expressions was attenuated by the treatments of memantine (P<0.01)). It was showed that Akt inhibitors LY294002 reversed the protective effects on neural stem cells proliferation by memantine(P<0.01). Conclusion The results suggest that memantine treatment might attenuate isofluane￣induced decrease of proliferation in neural stem cells via Akt signaling pathway.