Hu Shuxian, Sheng Wen S, Lokensgard James R, Peterson Phillip K
Division of Infectious Diseases and International Medicine, University of Minnesota Medical School, Minneapolis, Minnesota, USA.
J Infect Dis. 2005 Mar 15;191(6):886-9. doi: 10.1086/427830. Epub 2005 Feb 10.
To investigate the effect of opiates on human immunodeficiency virus type 1 (HIV-1)-related neuronal apoptosis, primary human fetal neuronal/glial cell cultures were exposed to gp120(IIIB) in the absence and the presence of morphine. Although morphine by itself had little effect on neuronal survival, the combination of morphine (>/=10(-7) mol/L) and gp120(IIIB) (1 nmol/L) significantly increased neuronal apoptosis. The mechanism whereby morphine potentiates gp120(IIIB)-induced neuronal apoptosis appears to involve activation of the p38 mitogen-activated protein kinase intracellular signaling pathway and microglial cells dispersed within the neuronal/glial cell cultures. These results provide additional insight into the molecular basis whereby opiate abuse could promote HIV-1-associated dementia.
为研究阿片类药物对1型人类免疫缺陷病毒（HIV-1）相关神经元凋亡的影响，将原代人胎儿神经元/神经胶质细胞培养物在不存在和存在吗啡的情况下暴露于gp120（IIIB）。虽然吗啡本身对神经元存活影响很小，但吗啡（≥10⁻⁷mol/L）和gp120（IIIB）（1 nmol/L）联合使用显著增加了神经元凋亡。吗啡增强gp120（IIIB）诱导的神经元凋亡的机制似乎涉及p38丝裂原活化蛋白激酶细胞内信号通路的激活以及分散在神经元/神经胶质细胞培养物中的小胶质细胞。这些结果为阿片类药物滥用可能促进HIV-1相关痴呆的分子基础提供了更多见解。
