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首页> 外文期刊>Molecular Neurobiology >Inhibition of Cyclooxygenase-2 (COX-2) Initiates Autophagy and Potentiates MPTP-Induced Autophagic Cell Death of Human Neuroblastoma Cells, SH-SY5Y: an Inside in the Pathology of Parkinson’s Disease
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Inhibition of Cyclooxygenase-2 (COX-2) Initiates Autophagy and Potentiates MPTP-Induced Autophagic Cell Death of Human Neuroblastoma Cells, SH-SY5Y: an Inside in the Pathology of Parkinson’s Disease

机译：环氧氧基酶-2（COX-2）的抑制引发了自噬和增强物体MPTP诱导的人神经母细胞瘤细胞的自噬细胞死亡，SH-SY5Y：帕金森病病理中的内部

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Cyclooxygenase-2 or COX-2 has been known to be crucial for Parkinson’s disease (PD) pathogenesis; however, its exact role is still not known. We first time report that inhibition of COX-2 promotes 1-methyl-4-phenyl 1,2,3,6 tetrahydropyridine (MPTP)-induced neuronal cell death via induction of autophagic mechanisms. We found that treatment with MPTP induced cell death of neuroblastoma cells SH-SY5Y in a dose dependent manner. Treatment of MPTP has also upregulated the expressions of autophagic proteins such as LC3, beclin, ATG-5, and p62. Interestingly, nimesulide, a preferential COX-2 inhibitor, further potentiated the MPTP-induced cell death of human neuroblastoma cells. Treatment of nimesulide with MPTP further potentiated expressions of p62, ATG-5, beclin-1, LC3 autophagic proteins. Furthermore, nimesulide with MPTP increased apoptotic protein cleaved caspase-3 and also induced expression of p53 gene. Interestingly, it was observed that Akt inhibitor significantly increased MPTP-induced cell death of neuroblastoma cells. However, (?) deprenyl, a monoamine oxidase B (MAO B) inhibitor, attenuated MPTP-induced autophagic response and protected cell death. The prior treatment with prostaglandin E2 protected against nimesulide induced-death of neuronal cells. This study confirms that neuroinflammation is associated to the autophagy and may be one of the main pathological mechanisms in Parkinson’s?disease and other inflammation-associated disorders.
机译：已知环氧杂酶-2或COX-2对帕金森病（PD）发病机制至关重要;但是，其确切的作用尚不清楚。我们首次报告COX-2的抑制促进1-甲基-4-苯基1,2,3,6四氢吡啶（MPTP）诱导的神经元细胞死亡通过诱导自噬机制。我们发现用剂量依赖性方式发现MPTP诱导神经母细胞瘤细胞的细胞死亡。 MPTP的治疗还上调了自噬蛋白如LC3，BEN1，ATG-5和P62的表达。有趣的是，Nimesulide是优先考虑的Cox-2抑制剂，进一步增强了人神经母细胞瘤细胞的MPTP诱导的细胞死亡。用MPTP处理P62，ATG-5，BECLIN-1，LC3自噬蛋白的MPTP进一步调节表达的Nimesulide。此外，Nimesulide与MPTP增加了凋亡蛋白切割的Caspase-3，也诱导了p53基因的表达。有趣的是，观察到AKT抑制剂显着增加了神经母细胞瘤细胞的MPTP诱导的细胞死亡。然而，（α）脱硫，单胺氧化酶B（MAO B）抑制剂，减毒的MPTP诱导的自噬响应和受保护的细胞死亡。前期治疗前列腺素E2免受神经元细胞的尼美诱导的抗死亡。本研究证实，神经引发与自噬相关，并且可能是帕金森的主要病理机制之一？疾病和其他炎症相关疾病。

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