Nolan Yvonne, Martin Darren, Campbell Veronica A, Lynch M A
Department of Anatomy/Neuroscience, University College, Cork, Ireland.
J Neuroimmunol. 2004 Jun;151(1-2):12-23. doi: 10.1016/j.jneuroim.2004.02.001.
Lipopolysaccharide (LPS) has a negative impact on long-term potentiation (LTP) in the rat hippocampus, which has been correlated with increased concentration of interleukin-1 beta (IL-1 beta) and activation of p38 and c-Jun N-terminal kinase (JNK). It has been documented that phosphatidylserine (PS)-containing liposomes induce anti-inflammatory signals and we report that pre-treatment of rats with PS liposomes prevented these LPS-induced effects while also inhibiting microglial activation. We also observed increased concentration of the anti-inflammatory cytokine interleukin-10 (IL-10), whose intracerebroventricular injection administration mimicked the effects of PS liposomes on LTP. This suggests that administration of PS liposomes protects against the deleterious effects of LPS possibly through generation of the anti-inflammatory cytokine IL-10.
脂多糖(LPS)对大鼠海马体的长时程增强(LTP)有负面影响,这与白细胞介素-1β(IL-1β)浓度升高以及p38和c-Jun氨基末端激酶(JNK)的激活有关。有文献记载,含磷脂酰丝氨酸(PS)的脂质体可诱导抗炎信号,我们报告称,用PS脂质体预处理大鼠可预防这些LPS诱导的效应,同时还能抑制小胶质细胞的激活。我们还观察到抗炎细胞因子白细胞介素-10(IL-10)的浓度增加,其脑室内注射给药模拟了PS脂质体对LTP的影响。这表明,PS脂质体给药可能通过产生抗炎细胞因子IL-10来保护机体免受LPS的有害影响。