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Effect of the PGD(2)-DP signaling pathway on primary cultured rat hippocampal neuron injury caused by aluminum overload

In the present study, the agonists and antagonists of DP receptor were used to examine whether the PGD(2)-DP signaling pathway affects neuronal function. Primary cultured hippocampal neuron was prepared and treated with aluminum maltolate (100 μM) to establish the neuronal damage model. PGD(2) and c...

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Autores principales: Ma, Jie, Yang, Qunfang, Wei, Yuling, Yang, Yang, Ji, Chaonan, Hu, Xinyue, Mai, Shaoshan, Kuang, Shengnan, Tian, Xiaoyan, Luo, Ying, Liang, Guojuan, Yang, Junqing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4835855/
https://www.ncbi.nlm.nih.gov/pubmed/27089935
http://dx.doi.org/10.1038/srep24646
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author Ma, Jie
Yang, Qunfang
Wei, Yuling
Yang, Yang
Ji, Chaonan
Hu, Xinyue
Mai, Shaoshan
Kuang, Shengnan
Tian, Xiaoyan
Luo, Ying
Liang, Guojuan
Yang, Junqing
author_facet Ma, Jie
Yang, Qunfang
Wei, Yuling
Yang, Yang
Ji, Chaonan
Hu, Xinyue
Mai, Shaoshan
Kuang, Shengnan
Tian, Xiaoyan
Luo, Ying
Liang, Guojuan
Yang, Junqing
author_sort Ma, Jie
collection PubMed
description In the present study, the agonists and antagonists of DP receptor were used to examine whether the PGD(2)-DP signaling pathway affects neuronal function. Primary cultured hippocampal neuron was prepared and treated with aluminum maltolate (100 μM) to establish the neuronal damage model. PGD(2) and cAMP content was detected by ELISA. L-PGDS and DPs mRNA and protein expression were measured by RT-PCR and Western blotting, respectively. The aluminium-load neuron was treated with the DP(1) agonist BW245C, the DP(1) antagonist BWA868C, the DP(2) agonist DK-PGD(2,) and the DP(2) antagonist CAY10471, respectively. Neuronal pathomorphology was observed using H-E staining. The cell viability and the lactate dehydrogenase leakage rates of neurons were measured with MTT and LDH kit, respectively. Ca(2+) level was detected by Fluo-3/AM. In the model group, the MTT values obviously decreased; LDH leakage rates and PGD(2) content increased significantly; L-PGDS, DP(1) mRNA and protein expressions increased, and DP(2) level decreased. BW245C reduced the Ca(2+) fluorescence intensity and protected the neurons. DK-PGD(2) increased the intensity of Ca(2+) fluorescence, while CAY10471 had the opposite effect. In conclusion, contrary to the effect of DP(2), the PGD(2)-DP(1) signaling pathway protects against the primary cultured rat hippocampal neuronal injury caused by aluminum overload.
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spelling pubmed-48358552016-04-27 Effect of the PGD(2)-DP signaling pathway on primary cultured rat hippocampal neuron injury caused by aluminum overload Ma, Jie Yang, Qunfang Wei, Yuling Yang, Yang Ji, Chaonan Hu, Xinyue Mai, Shaoshan Kuang, Shengnan Tian, Xiaoyan Luo, Ying Liang, Guojuan Yang, Junqing Sci Rep Article In the present study, the agonists and antagonists of DP receptor were used to examine whether the PGD(2)-DP signaling pathway affects neuronal function. Primary cultured hippocampal neuron was prepared and treated with aluminum maltolate (100 μM) to establish the neuronal damage model. PGD(2) and cAMP content was detected by ELISA. L-PGDS and DPs mRNA and protein expression were measured by RT-PCR and Western blotting, respectively. The aluminium-load neuron was treated with the DP(1) agonist BW245C, the DP(1) antagonist BWA868C, the DP(2) agonist DK-PGD(2,) and the DP(2) antagonist CAY10471, respectively. Neuronal pathomorphology was observed using H-E staining. The cell viability and the lactate dehydrogenase leakage rates of neurons were measured with MTT and LDH kit, respectively. Ca(2+) level was detected by Fluo-3/AM. In the model group, the MTT values obviously decreased; LDH leakage rates and PGD(2) content increased significantly; L-PGDS, DP(1) mRNA and protein expressions increased, and DP(2) level decreased. BW245C reduced the Ca(2+) fluorescence intensity and protected the neurons. DK-PGD(2) increased the intensity of Ca(2+) fluorescence, while CAY10471 had the opposite effect. In conclusion, contrary to the effect of DP(2), the PGD(2)-DP(1) signaling pathway protects against the primary cultured rat hippocampal neuronal injury caused by aluminum overload. Nature Publishing Group 2016-04-19 /pmc/articles/PMC4835855/ /pubmed/27089935 http://dx.doi.org/10.1038/srep24646 Text en Copyright © 2016, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
spellingShingle Article
Ma, Jie
Yang, Qunfang
Wei, Yuling
Yang, Yang
Ji, Chaonan
Hu, Xinyue
Mai, Shaoshan
Kuang, Shengnan
Tian, Xiaoyan
Luo, Ying
Liang, Guojuan
Yang, Junqing
Effect of the PGD(2)-DP signaling pathway on primary cultured rat hippocampal neuron injury caused by aluminum overload
title Effect of the PGD(2)-DP signaling pathway on primary cultured rat hippocampal neuron injury caused by aluminum overload
title_full Effect of the PGD(2)-DP signaling pathway on primary cultured rat hippocampal neuron injury caused by aluminum overload
title_fullStr Effect of the PGD(2)-DP signaling pathway on primary cultured rat hippocampal neuron injury caused by aluminum overload
title_full_unstemmed Effect of the PGD(2)-DP signaling pathway on primary cultured rat hippocampal neuron injury caused by aluminum overload
title_short Effect of the PGD(2)-DP signaling pathway on primary cultured rat hippocampal neuron injury caused by aluminum overload
title_sort effect of the pgd(2)-dp signaling pathway on primary cultured rat hippocampal neuron injury caused by aluminum overload
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4835855/
https://www.ncbi.nlm.nih.gov/pubmed/27089935
http://dx.doi.org/10.1038/srep24646
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