COX-2-deficient mice are less prone to MPTP-neurotoxicity than wild-type mice
COX-2-deficient mice are less prone to MPTP-neurotoxicity than wild-type mice
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DOI：
10.1097/00001756-200310270-00009
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发表时间：
2003-10-27
期刊：
影响因子：
1.7
通讯作者：
Ho, SL
中科院分区：
文献类型：
--
作者：
Feng, ZH;Li, DD;Ho, SL
帕金森病的主要损害是黑质多巴胺能神经元的死亡。利用环氧合酶-2基因敲除小鼠，探讨环氧合酶-2在帕金森病发病机制中的作用。COX-2基因杂合子小鼠注射1-甲基-4-苯基-1，2，3，6-四氢吡啶(MPTP，一种已知可导致人类帕金森病的化学物质)后的死亡率低于野生型小鼠。MPTP处理的野生型小鼠黑质致密部酪氨酸羟化酶免疫反应神经元的数量比杂合子小鼠减少的幅度更大。抑制COX-2蛋白表达可减轻MPTP对黑质致密部多巴胺能神经元的损伤。这一结果提示抑制COX-2具有潜在的治疗意义。
The primary lesion in Parkinson's disease is the death of dopaminergic neurons in the substantia nigra. The role of cyclooxygenase (COX)-2 in the etiology of Parkinson's disease was explored using COX-2 gene knockout mice. Mortality after injection of 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP, a chemical known to cause parkinsonism in humans) in heterozygous COX-2-deficient mice was lower than that in wild-type mice. The number of tyrosine hydroxylase immunoreactive neurons in the substantia nigra pars compacta of MPTP-treated wild-type mice declined to a greater extent than in heterozygous mice. Inhibition of COX-2 protein expression decreased the lesion caused by MPTP and protected the dopaminergic neurons in substantia nigra pars compacta. This result suggested that inhibition of COX-2 has potential therapeutic implications.