广州医药
廣州醫藥
엄주의약
GUANGZHOU MEDICAL JOURNAL
2014年
5期
4-7
,共4页
神经生长因子%PI3K/Akt 信号通路%少突胶质细胞%早产%大鼠
神經生長因子%PI3K/Akt 信號通路%少突膠質細胞%早產%大鼠
신경생장인자%PI3K/Akt 신호통로%소돌효질세포%조산%대서
Nerve growth factor%PI3K/Akt signaling pathway%Oligodendrocytes%Premature%Rat
目的探讨在脑室周围白质软化的早产大鼠中，脑组织 PI3K/Akt 通路的磷酸化激活情况，以及神经生长因子是否有抗少突胶质细胞凋亡的作用。方法本实验研究在早产大鼠脑室周围白质软化后，脑组织中少突胶质细胞的凋亡情况。给予神经生长因子，比较脑组织中 Akt 磷酸化激活情况及相应少突胶质细胞凋亡改变。结果早产大鼠脑损伤后，脑组织中少突胶质细胞凋亡急剧增加，给予神经生长因子后，脑组织中 Akt 磷酸化激活明显增加，相应少突胶质细胞凋亡明显减少。结论神经生长因子对脑损伤的保护机制与其增强 PI3K/Akt 信号转导通路的激活有关，激活 PI3K/Akt 信号转导通路可防治脑损伤刺激后的少突胶质细胞的凋亡。
目的探討在腦室週圍白質軟化的早產大鼠中，腦組織 PI3K/Akt 通路的燐痠化激活情況，以及神經生長因子是否有抗少突膠質細胞凋亡的作用。方法本實驗研究在早產大鼠腦室週圍白質軟化後，腦組織中少突膠質細胞的凋亡情況。給予神經生長因子，比較腦組織中 Akt 燐痠化激活情況及相應少突膠質細胞凋亡改變。結果早產大鼠腦損傷後，腦組織中少突膠質細胞凋亡急劇增加，給予神經生長因子後，腦組織中 Akt 燐痠化激活明顯增加，相應少突膠質細胞凋亡明顯減少。結論神經生長因子對腦損傷的保護機製與其增彊 PI3K/Akt 信號轉導通路的激活有關，激活 PI3K/Akt 信號轉導通路可防治腦損傷刺激後的少突膠質細胞的凋亡。
목적탐토재뇌실주위백질연화적조산대서중，뇌조직 PI3K/Akt 통로적린산화격활정황，이급신경생장인자시부유항소돌효질세포조망적작용。방법본실험연구재조산대서뇌실주위백질연화후，뇌조직중소돌효질세포적조망정황。급여신경생장인자，비교뇌조직중 Akt 린산화격활정황급상응소돌효질세포조망개변。결과조산대서뇌손상후，뇌조직중소돌효질세포조망급극증가，급여신경생장인자후，뇌조직중 Akt 린산화격활명현증가，상응소돌효질세포조망명현감소。결론신경생장인자대뇌손상적보호궤제여기증강 PI3K/Akt 신호전도통로적격활유관，격활 PI3K/Akt 신호전도통로가방치뇌손상자격후적소돌효질세포적조망。
Objective To explore activating phosphorylation of PI3K/Akt pathway in brain tissue and whether nerve growth factor has the effect of anti oligodendrocytes apoptosis in preterm rat with periventricular leukomalacia. Methods We studied apoptotic oligodendrocytes in brain tissue of preterm rats with periventricular leukomalacia and compared the situation of Akt phosphorylation activation and oligodendrocytes apoptosis change accordingly after nerve growth factor administered. Re-sults Oligodendrocytes apoptosis increased sharply in brain tissue after premature rats suffering periventricular leukomalacia.Akt phosphorylation activation increased significantly in brain tissue and the corresponding oligodendrocytes apoptosis decreased significantly after nerve growth factor administerd. Conclusion The effects of nerve growth factor on brain injury protection mechanism were related with enhancing the activation of PI3K/Akt signal transduction pathway.The activation of PI3K/Akt sig-nal transduction pathway may prevent and treat apoptotic oligodendrocytes after brain injury.
