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Hippocampal neuronal cyclooxygenase-2 downstream signaling imbalance in a rat model of chronic aluminium gluconate administration

机译:慢性葡萄糖酸铝给药大鼠模型中海马神经元环氧合酶-2下游信号不平衡

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摘要

BackgroundAcute and chronic brain damages including neurodegenerative diseases are a group of neuroinflammation-associated diseases characterized by cognitive function defect and progressive neuron loss. The pathophysiological procession of brain damages involves the overexpression of cyclooxygenase (COX)-2. Owing to the limited benefit to chronic brain damage and the late adverse effect of COX-2 inhibitors, the COX downstream signaling pathway has become a focus in neurological research. In order to explore the mechanism of aluminum neurotoxicity and the importance of COX2 downstream signaling pathways to chronic brain damage, the present study was designed to simultaneously observe the prostaglandin (PG) contents, and the expressions of PG synthases and PG receptors of hippocampus in a rat model induced by chronic administration of aluminium gluconate.
机译:背景技术包括神经退行性疾病在内的急性和慢性脑损伤是一组以认知功能缺陷和进行性神经元丧失为特征的神经炎症相关疾病。脑损伤的病理生理过程涉及环氧合酶(COX)-2的过表达。由于对慢性脑损伤的益处有限以及COX-2抑制剂的后期不良作用,COX下游信号通路已成为神经学研究的重点。为了探讨铝神经毒性的机制以及COX2下游信号通路对慢性脑损伤的重要性,本研究旨在同时观察前列腺素(PG)的含量以及海马中PG合成酶和PG受体的表达。长期施用葡萄糖酸铝诱导的大鼠模型。

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