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231225s2021 xx |||||o 00| ||eng c |
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|a 10.1155/2021/8851327
|2 doi
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|a eng
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| 100 |
1 |
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|a Xue, Xiangli
|e verfasserin
|4 aut
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| 245 |
1 |
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|a Interactions between Endoplasmic Reticulum Stress and Autophagy
|b Implications for Apoptosis and Neuroplasticity-Related Proteins in Palmitic Acid-Treated Prefrontal Cells
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|c 2021
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
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|a ƒa Online-Ressource
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|a Date Completed 02.03.2022
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|a Date Revised 02.03.2022
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|a published: Electronic-eCollection
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|a Citation Status MEDLINE
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|a Copyright © 2021 Xiangli Xue et al.
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|a Lipotoxicity of palmitic acid (PA) or high-fat diets has been reported to increase endoplasmic reticulum (ER) stress and autophagy in peripheral tissue as well as apoptotic cell death. It also can lead to an AD-like pathological pattern. However, it has been unknown that PA-induced ER stress and autophagy are involved in the regulation of neuroplastic abnormalities. Here, we investigated the roles of ER stress and autophagy in apoptosis and neuroplasticity-related protein expression in PA-treated prefrontal cells. Prefrontal cells dissected from newborn Sprague-Dawley rats were treated with PA compound with ER stress inhibitor 4-phenylbutyric acid (4-PBA) and autophagy inhibitor 3-methyladenine (3-MA) or PA alone. PA promoted ER stress and autophagy and also cause apoptosis as well as a decline in the expression of neuroplasticity-related proteins. Inhibition of ER stress decreased the expressions of neuroplasticity-related proteins and reduced autophagy activation and apoptosis in PA-treated prefrontal cells. Inhibition of autophagy exacerbated apoptosis and enhanced ER stress in PA-treated prefrontal cells. The present study illustrated that both ER stress and autophagy could be involved in apoptosis and decreased neuroplasticity-related proteins, and the interaction between ER stress and autophagy may play a critical role in apoptosis in PA-treated prefrontal cells. Our results provide new insights into the molecular mechanisms in vitro of lipotoxicity in obesity-related cognitive dysfunction
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|a Journal Article
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| 650 |
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|a Research Support, Non-U.S. Gov't
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| 650 |
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|a Enzyme Inhibitors
|2 NLM
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| 650 |
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|a Palmitic Acid
|2 NLM
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| 650 |
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7 |
|a 2V16EO95H1
|2 NLM
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| 700 |
1 |
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|a Li, Feng
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Cai, Ming
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Hu, Jingyun
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Wang, Qian
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Lou, Shujie
|e verfasserin
|4 aut
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| 773 |
0 |
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|i Enthalten in
|t Neural plasticity
|d 1998
|g 2021(2021) vom: 11., Seite 8851327
|w (DE-627)NLM098558390
|x 1687-5443
|7 nnns
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| 773 |
1 |
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|g volume:2021
|g year:2021
|g day:11
|g pages:8851327
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| 856 |
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|u http://dx.doi.org/10.1155/2021/8851327
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