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环氧化酶-2 信号通路在皮质中的作用涉及抑郁大鼠模型中的病理生理机制。

Cyclooxygenase-2 Signalling Pathway in the Cortex is Involved in the Pathophysiological Mechanisms in the Rat Model of Depression.

机构信息

Department of Pharmacology, Chongqing Medical University, the Key Laboratory of Biochemistry and Molecular Pharmacology, Chongqing, 400016, China.

出版信息

Sci Rep. 2017 Mar 28;7(1):488. doi: 10.1038/s41598-017-00609-7.

DOI:10.1038/s41598-017-00609-7
PMID:28352129
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5428817/
Abstract

This study was designed to investigate the effect of the cortical cyclooxygenase-2 (COX2) pathway on depressive behaviour in rats. Meloxicam, COX2 overexpressed lentivirus and COX2 RNAi lentivirus were administered to Sprague-Dawley rats subjected to chronic unpredictable mild stress (CUMS). Behaviour tests, biochemistry and immunohistochemistry methods, enzyme-linked immunosorbent assays, western blotting and reverse transcription polymerase chain reactions were used to evaluate the changes in rat behaviour and the cortical COX2 pathway. CUMS rats showed depressive-like behaviours. The superoxide dismutase activity and cyclic adenosine monophosphate (cAMP) contents were significantly decreased, the contents of malondialdehyde, prostaglandin E2 (PGE2) and inflammatory cytokines were significantly increased. The expressions of protein kinase A (PKA) and cAMP response element-binding protein (CREB) were decreased, and the levels of brain-derived neurotrophic factor (BDNF) and COX2 were significantly increased. Meloxicam and COX2 RNAi lentivirus significantly alleviated the abnormalities induced by CUMS, while COX2 overexpressed lentivirus aggravated these abnormalities. Our results indicated that the cortical COX2 pathway was activated in CUMS rats. Inhibition of COX2 activity/expression can obviously improve depressive behaviours in CUMS rats. Upregulating COX2 expression can increase the susceptibility of rats to CUMS. An imbalance in the cortical COX2-PGE2-cAMP/PKA-CREB-BDNF signalling pathway participates in the pathogenic mechanism of depression.

摘要

本研究旨在探讨皮质环氧化酶-2（COX2）通路对大鼠抑郁行为的影响。将美洛昔康、过表达 COX2 的慢病毒和 COX2 RNAi 慢病毒给予慢性不可预测轻度应激（CUMS）大鼠。采用行为测试、生物化学和免疫组织化学方法、酶联免疫吸附测定法、western blot 法和逆转录聚合酶链反应评估大鼠行为和皮质 COX2 通路的变化。CUMS 大鼠表现出类似抑郁的行为。超氧化物歧化酶活性和环磷酸腺苷（cAMP）含量明显降低，丙二醛、前列腺素 E2（PGE2）和炎性细胞因子含量明显升高。蛋白激酶 A（PKA）和 cAMP 反应元件结合蛋白（CREB）的表达减少，脑源性神经营养因子（BDNF）和 COX2 的水平明显增加。美洛昔康和 COX2 RNAi 慢病毒明显缓解了 CUMS 引起的异常，而过表达 COX2 的慢病毒则加重了这些异常。我们的结果表明，CUMS 大鼠皮质 COX2 通路被激活。抑制 COX2 活性/表达能明显改善 CUMS 大鼠的抑郁行为。上调 COX2 表达可增加大鼠对 CUMS 的易感性。皮质 COX2-PGE2-cAMP/PKA-CREB-BDNF 信号通路的失衡参与了抑郁症的发病机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c19/5428817/99114acb9257/41598_2017_609_Fig8_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c19/5428817/99114acb9257/41598_2017_609_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c19/5428817/f6b78012f266/41598_2017_609_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c19/5428817/6ef316709256/41598_2017_609_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c19/5428817/7207ca8170f1/41598_2017_609_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c19/5428817/58d74f27dd17/41598_2017_609_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c19/5428817/2fc2b8b77b29/41598_2017_609_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c19/5428817/de85aeb80008/41598_2017_609_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c19/5428817/9974b6387dbd/41598_2017_609_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c19/5428817/99114acb9257/41598_2017_609_Fig8_HTML.jpg

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