摘要
目的为了探讨酪氨酸蛋白激酶抑制剂Genistein对人类免疫缺陷病毒Ⅰ型(HIV1)的包膜糖蛋白gp120引起大鼠海马脑片CA1区的长时程增强效应(Longtermpotentiation,LTP)作用的影响。方法应用离体脑片记录技术,记录大鼠海马CA1区的兴奋性突触后电位EPSP,研究了Genistein对gp120引起的大鼠海马脑片CA1区的突触传递和可塑性变化的影响。结果gp120对高频电刺激(HFS,100Hz,1000ms×2,串间隔20s,共2次)Schaffer侧支引起的大鼠海马CA1区LTP产生抑制作用,而对PTP没有影响。酪氨酸蛋白激酶抑制剂Genistein可以反转这种抑制效应。结论gp120可能通过抑制海马CA1区LTP而参与艾滋病痴呆(HIV1associateddementia,HAD)的形成,且这种抑制作用可能与酪氨酸蛋白激酶抑制剂Genistein有关。
Objective To explore the effect of tyrosine kinase inhibitor genistein on long-term potentiation (LTP) inhibited by HIV-1gp120 in the CA1 region of rat hippocampal slices. Methods The excitatory postsynaptic potentials (EPSP) and the effect of genistein on gpl20-induced synaptic transmission and plastic change were recorded and investigated in the CA, region of rat hippocampal slices. Results The results showed that HIV-1 gp120 could inhibit the LTP of CA1, but not the PTP. Protein kinase inhibitor genistein could reverse the inhibitory effect. Conclusion The effect of tyrosine kinase inhibitor genistein on long-term potentiation inhibited by HIV-1gp120 may contribute to the HAD pathogenesis.
出处
《免疫学杂志》
CAS
CSCD
北大核心
2005年第6期485-488,共4页
Immunological Journal
基金
广东省医学科研基金项目(A2004327)
广东省自然科学基金项目(04010443)
国家中管局择优项目(国中医药科2003LHR13号)
国家中管局三A重点实验室开放课题基金项目(51205026)资助