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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >The role of Ca2+ channel modulation in the neuroprotective actions of estrogen in beta-amyloid protein and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) cytotoxic models.
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The role of Ca2+ channel modulation in the neuroprotective actions of estrogen in beta-amyloid protein and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) cytotoxic models.

机译：Ca2 +通道调节在β-淀粉样蛋白和1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）细胞毒性模型中雌激素的神经保护作用中的作用。

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Physiologically relevant concentrations of 17beta-estradiol (E2) are neuroprotective in both beta-amyloid protein 25-35 (Abeta) and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induced cytotoxicity in SK-N-SH cells. MPTP, but not Abeta, induces apoptosis in this cell line. The L-type calcium channel blocker nifedipine or decreased extracellular Ca(2+) concentration blocked Abeta-induced cell death, but not MPTP-induced cell death. Other blockers selective for different Ca(2+) channel subtypes had no effects on either Abeta or MPTP induced death. Western blot analysis for L-type Ca(2+) channel alpha(1)-subunits demonstrated that Abeta increases the expression of the neuronal alpha(1C) and alpha(1D) subunits of L-type channels. Both E2 and nifedipine inhibit the increase in expression of these by Abeta. MPTP also increases expression of alpha(1C) and alpha(1D), but the increases were not influenced by E2 or nifedipine. These observations suggested that Abeta cytotoxicity in SK-N-SH cells may involve increased availability of calcium to cells, whereas MPTP induced cytotoxicity does not require extracellular Ca(2+). Both cytotoxic models were associated with increased expression of Ca(2+) channel alpha(1) subunits, and neuroprotection associated with inhibition of that increase. These studies reveal that nifedipine, in addition to its direct action of nifedipine on Ca(2+) channels, may also protect neurons from Abeta toxicity through the suppression of the channel protein overexpression. A new action of dihydropyridines (DHPs) may be considered in the regulation of calcium homeostasis.
机译：生理相关浓度的17β-雌二醇（E2）在β-淀粉样蛋白25-35（Abeta）和1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）诱导的SK-细胞毒性中均具有神经保护作用。 N-SH细胞。 MPTP而非Abeta诱导该细胞系凋亡。 L型钙通道阻滞剂硝苯地平或降低的细胞外Ca（2+）浓度阻止Abeta诱导的细胞死亡，但不是MPTP诱导的细胞死亡。对不同的Ca（2+）通道亚型有选择性的其他阻滞剂对Abeta或MPTP诱导的死亡均无影响。对L型Ca（2+）通道alpha（1）-亚基的蛋白质印迹分析表明，Abeta增加了L型通道的神经元alpha（1C）和alpha（1D）亚基的表达。 E2和硝苯地平均通过Abeta抑制其表达的增加。 MPTP还增加了alpha（1C）和alpha（1D）的表达，但增加不受E2或硝苯地平的影响。这些观察结果表明，SK-N-SH细胞中的Abeta细胞毒性可能涉及增加钙对细胞的利用率，而MPTP诱导的细胞毒性不需要细胞外Ca（2+）。两种细胞毒性模型都与Ca（2+）通道alpha（1）亚基的表达增加有关，而神经保护作用与抑制这种增加有关。这些研究表明硝苯地平，除了硝苯地平对Ca（2+）通道的直接作用，还可以通过抑制通道蛋白的过表达来保护神经元免受Abeta毒性。二氢吡啶（DHP）的新作用可考虑调节钙稳态。

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