The Absence of Nrf2 Enhances NF-B-Dependent Inflammation following Scratch Injury in Mouse Primary Cultured Astrocytes
It has been proved that Nrf2 depletion enhances inflammatory process through activation of NF-κB in the brain after TBI, but little is known about the relationship between Nrf2 and NF-κB in astrocytes after TBI. Hence, we used primary cultured astrocytes from either Nrf2 wildtype or knockout mice to...
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| Format: | Article |
| Language: | English |
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Wiley
2012-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2012/217580 |
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| author | Hao Pan Handong Wang Xiaoliang Wang Lin Zhu Lei Mao |
| author_facet | Hao Pan Handong Wang Xiaoliang Wang Lin Zhu Lei Mao |
| author_sort | Hao Pan |
| collection | DOAJ |
| description | It has been proved that Nrf2 depletion enhances inflammatory process through activation of NF-κB in the brain after TBI, but little is known about the relationship between Nrf2 and NF-κB in astrocytes after TBI. Hence, we used primary cultured astrocytes from either Nrf2 wildtype or knockout mice to study the influence of Nrf2 on the activation of NF-κB and expression of proinflammatory cytokines in a model of TBI in vitro. Primary cultured astrocytes were scratched to mimic the traumatic injury in vitro. Then the DNA-binding activity of NF-κB was evaluated by EMSA. The mRNA and protein levels of TNF-α, IL-1β, IL-6, and MMP9 were also evaluated. Gelatin zymography was performed to detect the activity of MMP9. The activity of NF-κB and expression of proinflammatory cytokines mentioned above were upregulated at 24 h after scratch. The expression and activity of MMP9 were also elevated. And such tendency was much more prominent in Nrf2 KO astrocytes than that in WT astrocytes. These results suggest that the absence of Nrf2 may induce more aggressive inflammation through activation of NF-κB and downstream proinflammatory cytokines in astrocytes. |
| format | Article |
| id | doaj-art-84a4d0339c4b4a46938d98755bd831eb |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2012-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-84a4d0339c4b4a46938d98755bd831eb2025-02-03T01:27:53ZengWileyMediators of Inflammation0962-93511466-18612012-01-01201210.1155/2012/217580217580The Absence of Nrf2 Enhances NF-B-Dependent Inflammation following Scratch Injury in Mouse Primary Cultured AstrocytesHao Pan0Handong Wang1Xiaoliang Wang2Lin Zhu3Lei Mao4Department of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, Jiangsu 210002, ChinaDepartment of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, Jiangsu 210002, ChinaDepartment of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, Jiangsu 210002, ChinaDepartment of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, Jiangsu 210002, ChinaDepartment of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, Jiangsu 210002, ChinaIt has been proved that Nrf2 depletion enhances inflammatory process through activation of NF-κB in the brain after TBI, but little is known about the relationship between Nrf2 and NF-κB in astrocytes after TBI. Hence, we used primary cultured astrocytes from either Nrf2 wildtype or knockout mice to study the influence of Nrf2 on the activation of NF-κB and expression of proinflammatory cytokines in a model of TBI in vitro. Primary cultured astrocytes were scratched to mimic the traumatic injury in vitro. Then the DNA-binding activity of NF-κB was evaluated by EMSA. The mRNA and protein levels of TNF-α, IL-1β, IL-6, and MMP9 were also evaluated. Gelatin zymography was performed to detect the activity of MMP9. The activity of NF-κB and expression of proinflammatory cytokines mentioned above were upregulated at 24 h after scratch. The expression and activity of MMP9 were also elevated. And such tendency was much more prominent in Nrf2 KO astrocytes than that in WT astrocytes. These results suggest that the absence of Nrf2 may induce more aggressive inflammation through activation of NF-κB and downstream proinflammatory cytokines in astrocytes.http://dx.doi.org/10.1155/2012/217580 |
| spellingShingle | Hao Pan Handong Wang Xiaoliang Wang Lin Zhu Lei Mao The Absence of Nrf2 Enhances NF-B-Dependent Inflammation following Scratch Injury in Mouse Primary Cultured Astrocytes Mediators of Inflammation |
| title | The Absence of Nrf2 Enhances NF-B-Dependent Inflammation following Scratch Injury in Mouse Primary Cultured Astrocytes |
| title_full | The Absence of Nrf2 Enhances NF-B-Dependent Inflammation following Scratch Injury in Mouse Primary Cultured Astrocytes |
| title_fullStr | The Absence of Nrf2 Enhances NF-B-Dependent Inflammation following Scratch Injury in Mouse Primary Cultured Astrocytes |
| title_full_unstemmed | The Absence of Nrf2 Enhances NF-B-Dependent Inflammation following Scratch Injury in Mouse Primary Cultured Astrocytes |
| title_short | The Absence of Nrf2 Enhances NF-B-Dependent Inflammation following Scratch Injury in Mouse Primary Cultured Astrocytes |
| title_sort | absence of nrf2 enhances nf b dependent inflammation following scratch injury in mouse primary cultured astrocytes |
| url | http://dx.doi.org/10.1155/2012/217580 |
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