Nuclear factor-κB activation is not involved in a MPTP model of Parkinson's disease

被引：30

作者：

Teismann, P

Schwaninger, M

Weih, F

Ferger, B

机构：

[1] Univ Marburg, Fac Pharm, Inst Pharmacol & Toxicol, D-35032 Marburg, Germany

[2] Univ Heidelberg, Dept Neurol, D-69120 Heidelberg, Germany

[3] Forschungszentrum Karlsruhe, Inst Toxicol & Genet, D-76021 Karlsruhe, Germany

来源：

NEUROREPORT | 2001年 / 12卷 / 05期

关键词：

hydroxyl radicals; microdialysis; MPTP; neurodegeneration; nuclear factor-kappa B; Parkinson's disease;

D O I：

10.1097/00001756-200104170-00037

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

In the present study the involvement of hydroxyl free radicals and nuclear factor-kappaB (NF-kappaB) activation was investigated in the MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) model of Parkinson's disease. MPTP (30 mg/kg, s.c.) produced a significant 2-fold increase in hydroxyl free radicals in the striatum of C57BL/6 mice determined by microdialysis in combination with the salicylate hydroxylation assay. Electrophoretic mobility shift assays did not detect NF-kappaB activation after MPTP treatment. Furthermore, p50-deficient mice showed only minor differences in striatal dopamine and metabolite levels as well as tyrosine hydroxylase immunoreactivity after MPTP administration in comparison to wildtype mice. We postulate that, although hydroxyl radical production was enhanced, NF-kappaB plays only a minor role in the MPTP model because neither neurochemical nor immunocytochemical parameters were altered in:p50-deficient mice in comparison to controls. NeuroReport 12:1049-1053 (C) 2001 Lippincott Williams & Wilkins.

引用

页码：1049 / 1053

页数：5

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