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Ginsenoside Rg1 protects against neuronal degeneration induced by chronic dexamethasone treatment by inhibiting NLRP-1 inflammasomes in mice
Glucocorticoids (GCs) are known to alter neuronal plasticity, impair learning and memory and play important roles in the generation and progression of Alzheimer's disease. There are no effective drug options for preventing neuronal injury induced by chronic GC exposure. Ginsenoside Rg1 (Rg1) is...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5593467/ https://www.ncbi.nlm.nih.gov/pubmed/28849171 http://dx.doi.org/10.3892/ijmm.2017.3092 |
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author | Zhang, Yaodong Hu, Wen Zhang, Biqiong Yin, Yanyan Zhang, Junyan Huang, Dake Huang, Rongrong Li, Weiping Li, Weizu |
author_facet | Zhang, Yaodong Hu, Wen Zhang, Biqiong Yin, Yanyan Zhang, Junyan Huang, Dake Huang, Rongrong Li, Weiping Li, Weizu |
author_sort | Zhang, Yaodong |
collection | PubMed |
description | Glucocorticoids (GCs) are known to alter neuronal plasticity, impair learning and memory and play important roles in the generation and progression of Alzheimer's disease. There are no effective drug options for preventing neuronal injury induced by chronic GC exposure. Ginsenoside Rg1 (Rg1) is a steroidal saponin found in ginseng. The present study investigated the neuroprotective effect of Rg1 on neuroinflammation damage induced by chronic dexamethasone (5 mg/kg for 28 days) exposure in male mice. Our results showed that Rg1 (2 and 4 mg/kg) treatment increased spontaneous motor activity and exploratory behavior in an open field test, and increased the number of entries into the new object zone in a novel object recognition test. Moreover, Rg1 (2 and 4 mg/kg) treatment significantly alleviated neuronal degeneration and increased MAP2 expression in the frontal cortex and hippocampus. Additionally, inhibition of NLRP-1 inflammasomes was also involved in the mechanisms underlying the effect of Rg1 on GC-induced neuronal injury. We found that Rg1 (2 and 4 mg/kg) treatment increased the expression of glucocorticosteroid receptor and decreased the expression of NLRP-1, ASC, caspase-1, caspase-5, IL-1β and IL-18 in the hippocampus in male mice. The present study indicates that Rg1 may have protective effects on neuroinflammation and neuronal injury induced by chronic GC exposure. |
format | Online Article Text |
id | pubmed-5593467 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-55934672017-09-22 Ginsenoside Rg1 protects against neuronal degeneration induced by chronic dexamethasone treatment by inhibiting NLRP-1 inflammasomes in mice Zhang, Yaodong Hu, Wen Zhang, Biqiong Yin, Yanyan Zhang, Junyan Huang, Dake Huang, Rongrong Li, Weiping Li, Weizu Int J Mol Med Articles Glucocorticoids (GCs) are known to alter neuronal plasticity, impair learning and memory and play important roles in the generation and progression of Alzheimer's disease. There are no effective drug options for preventing neuronal injury induced by chronic GC exposure. Ginsenoside Rg1 (Rg1) is a steroidal saponin found in ginseng. The present study investigated the neuroprotective effect of Rg1 on neuroinflammation damage induced by chronic dexamethasone (5 mg/kg for 28 days) exposure in male mice. Our results showed that Rg1 (2 and 4 mg/kg) treatment increased spontaneous motor activity and exploratory behavior in an open field test, and increased the number of entries into the new object zone in a novel object recognition test. Moreover, Rg1 (2 and 4 mg/kg) treatment significantly alleviated neuronal degeneration and increased MAP2 expression in the frontal cortex and hippocampus. Additionally, inhibition of NLRP-1 inflammasomes was also involved in the mechanisms underlying the effect of Rg1 on GC-induced neuronal injury. We found that Rg1 (2 and 4 mg/kg) treatment increased the expression of glucocorticosteroid receptor and decreased the expression of NLRP-1, ASC, caspase-1, caspase-5, IL-1β and IL-18 in the hippocampus in male mice. The present study indicates that Rg1 may have protective effects on neuroinflammation and neuronal injury induced by chronic GC exposure. D.A. Spandidos 2017-10 2017-08-09 /pmc/articles/PMC5593467/ /pubmed/28849171 http://dx.doi.org/10.3892/ijmm.2017.3092 Text en Copyright: © Zhang et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Zhang, Yaodong Hu, Wen Zhang, Biqiong Yin, Yanyan Zhang, Junyan Huang, Dake Huang, Rongrong Li, Weiping Li, Weizu Ginsenoside Rg1 protects against neuronal degeneration induced by chronic dexamethasone treatment by inhibiting NLRP-1 inflammasomes in mice |
title | Ginsenoside Rg1 protects against neuronal degeneration induced by chronic dexamethasone treatment by inhibiting NLRP-1 inflammasomes in mice |
title_full | Ginsenoside Rg1 protects against neuronal degeneration induced by chronic dexamethasone treatment by inhibiting NLRP-1 inflammasomes in mice |
title_fullStr | Ginsenoside Rg1 protects against neuronal degeneration induced by chronic dexamethasone treatment by inhibiting NLRP-1 inflammasomes in mice |
title_full_unstemmed | Ginsenoside Rg1 protects against neuronal degeneration induced by chronic dexamethasone treatment by inhibiting NLRP-1 inflammasomes in mice |
title_short | Ginsenoside Rg1 protects against neuronal degeneration induced by chronic dexamethasone treatment by inhibiting NLRP-1 inflammasomes in mice |
title_sort | ginsenoside rg1 protects against neuronal degeneration induced by chronic dexamethasone treatment by inhibiting nlrp-1 inflammasomes in mice |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5593467/ https://www.ncbi.nlm.nih.gov/pubmed/28849171 http://dx.doi.org/10.3892/ijmm.2017.3092 |
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