Activation of TLR4-Mediated NF𝜅B Signaling in Hemorrhagic Brain in Rats
Inflammation and immunity play a crucial role in the pathogenesis of Intracerebral hemorrhage (ICH). Toll-like receptor 4- (TLR4-) mediated nuclear factor kappa-B (NF𝜅B) signaling plays critical roles in the activation and regulation of inflammatory responses in injured brain. However, the involveme...
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| Format: | Article |
| Language: | English |
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Wiley
2009-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2009/473276 |
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| author | Weiyu Teng Lishu Wang Weishuang Xue Chao Guan |
| author_facet | Weiyu Teng Lishu Wang Weishuang Xue Chao Guan |
| author_sort | Weiyu Teng |
| collection | DOAJ |
| description | Inflammation and immunity play a crucial role in the pathogenesis of Intracerebral hemorrhage (ICH). Toll-like receptor 4- (TLR4-) mediated nuclear factor kappa-B (NF𝜅B) signaling plays critical roles in the activation and regulation of inflammatory responses in injured brain. However, the involvement of TLR4-mediated NF𝜅B signaling in the pathogenesis of ICH remains unknown. The present study was to evaluate the temporal profile of the expression of TLR4 and the activation of TLR4-mediated NF𝜅B signaling in brain tissues of Wistar rats after ICH. TLR4 mRNA and protein, the phosphorylation of inhibitors of kappa B (p-I𝜅B𝛼), and the activity of NF𝜅B were examined in hemorrhagic cerebral tissue by Rt-PCR, Western blots, immunohistochemistry staining, and EMSA. Compared with saline control, the TLR4 mRNA and protein significantly increased starting at 6 hours after ICH, peaked on the 3rd day after ICH, and then decreased but still maintained at a higher level on the 7th day after ICH (𝑃<.05). The level of p-I𝜅B𝛼 and the activity of NF𝜅B also increased in the brain after ICH compared with saline control. The present study firstly suggests that TLR4-mediated NF𝜅B signaling participates in the pathogenesis of ICH, which may become a therapeutic target for ICH-induced brain damage. |
| format | Article |
| id | doaj-art-e8719c582be64f8faa261da632e88d18 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2009-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-e8719c582be64f8faa261da632e88d182025-02-03T01:21:48ZengWileyMediators of Inflammation0962-93511466-18612009-01-01200910.1155/2009/473276473276Activation of TLR4-Mediated NF𝜅B Signaling in Hemorrhagic Brain in RatsWeiyu Teng0Lishu Wang1Weishuang Xue2Chao Guan3Department of Neurology, The First Affiliated Hospital, China Medical University, Shenyang 110001, ChinaDepartment of Neurology, The First Affiliated Hospital, China Medical University, Shenyang 110001, ChinaDepartment of Neurology, The First Affiliated Hospital, China Medical University, Shenyang 110001, ChinaDepartment of Otorhinolaryngology, The First Affiliated Hospital, China Medical University, Shenyang 110001, ChinaInflammation and immunity play a crucial role in the pathogenesis of Intracerebral hemorrhage (ICH). Toll-like receptor 4- (TLR4-) mediated nuclear factor kappa-B (NF𝜅B) signaling plays critical roles in the activation and regulation of inflammatory responses in injured brain. However, the involvement of TLR4-mediated NF𝜅B signaling in the pathogenesis of ICH remains unknown. The present study was to evaluate the temporal profile of the expression of TLR4 and the activation of TLR4-mediated NF𝜅B signaling in brain tissues of Wistar rats after ICH. TLR4 mRNA and protein, the phosphorylation of inhibitors of kappa B (p-I𝜅B𝛼), and the activity of NF𝜅B were examined in hemorrhagic cerebral tissue by Rt-PCR, Western blots, immunohistochemistry staining, and EMSA. Compared with saline control, the TLR4 mRNA and protein significantly increased starting at 6 hours after ICH, peaked on the 3rd day after ICH, and then decreased but still maintained at a higher level on the 7th day after ICH (𝑃<.05). The level of p-I𝜅B𝛼 and the activity of NF𝜅B also increased in the brain after ICH compared with saline control. The present study firstly suggests that TLR4-mediated NF𝜅B signaling participates in the pathogenesis of ICH, which may become a therapeutic target for ICH-induced brain damage.http://dx.doi.org/10.1155/2009/473276 |
| spellingShingle | Weiyu Teng Lishu Wang Weishuang Xue Chao Guan Activation of TLR4-Mediated NF𝜅B Signaling in Hemorrhagic Brain in Rats Mediators of Inflammation |
| title | Activation of TLR4-Mediated NF𝜅B Signaling in Hemorrhagic Brain in Rats |
| title_full | Activation of TLR4-Mediated NF𝜅B Signaling in Hemorrhagic Brain in Rats |
| title_fullStr | Activation of TLR4-Mediated NF𝜅B Signaling in Hemorrhagic Brain in Rats |
| title_full_unstemmed | Activation of TLR4-Mediated NF𝜅B Signaling in Hemorrhagic Brain in Rats |
| title_short | Activation of TLR4-Mediated NF𝜅B Signaling in Hemorrhagic Brain in Rats |
| title_sort | activation of tlr4 mediated nf𝜅b signaling in hemorrhagic brain in rats |
| url | http://dx.doi.org/10.1155/2009/473276 |
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