Navarra M, Romano C, Lorenzon T, Rotiroti D, Di Renzo G
Department of Pharmacobiological Sciences, Faculty of Pharmacy, University of Catanzaro Magna Graecia & IBAF-CNR, 88021 Roccelletta di Borgia, Catanzaro, Italy.
J Neurosci Res. 2001 Aug 15;65(4):354-61. doi: 10.1002/jnr.1161.
The aim of present study was to investigate the acute effects of ethanol on cytotoxicity induced by HIV-1 coat protein gp120 in CHP100 human neuroblastoma cell line. We demonstrate that ethanol, within a range of clinically relevant concentrations (15-90 mM) prevents cell death elicited by gp120 (10 pM) in a dose dependent manner. This protective action seems to be mediated by a reduction of free intracellular Ca(2+) levels because ethanol, at concentrations ranging from 0.1-0.5%, is able to decrease gp120-stimulated Ca(2+) uptake up to 24%. Furthermore, our data show an involvement of NO/cGMP messenger system pathway, because ethanol is also able to reduce gp120-stimulated NO release (up to 45%) and cyclic GMP accumulation (up to 73%). These findings suggest that the protective effect of ethanol against gp120-induced cytotoxicity in CHP100 cells underlies a Ca(2+)-activated, NO/cGMP-dependent mechanism.
本研究的目的是调查乙醇对HIV-1包膜蛋白gp120在CHP100人神经母细胞瘤细胞系中诱导的细胞毒性的急性影响。我们证明，在一系列临床相关浓度（15 - 90 mM）范围内，乙醇以剂量依赖的方式防止gp120（10 pM）引发的细胞死亡。这种保护作用似乎是由细胞内游离Ca(2+)水平的降低介导的，因为浓度范围为0.1 - 0.5%的乙醇能够将gp120刺激的Ca(2+)摄取减少高达24%。此外，我们的数据表明NO/cGMP信使系统途径参与其中，因为乙醇还能够减少gp120刺激的NO释放（高达45%）和环鸟苷酸积累（高达73%）。这些发现表明，乙醇对CHP100细胞中gp120诱导的细胞毒性的保护作用基于一种Ca(2+)激活的、NO/cGMP依赖的机制。
