Oxymatrine Downregulates TLR4, TLR2, MyD88, and NF-κB and Protects Rat Brains against Focal Ischemia
Inflammatory damage plays an important role in cerebral ischemic pathogenesis and may represent a target for treatment. Toll-like receptor-4 (TLR4), toll-like receptor-2 (TLR2), myeloid differentiation factor 88 (MyD88), and nuclear factor kappa-B (NF-κB) have been linked to inflammatory reactions....
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| Main Authors: | , , , , , , |
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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/10.1155/2009/704706 |
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| author | Hongguang Fan Litao Li Xiangjian Zhang Ying Liu Chenhui Yang Yi Yang Jing Yin |
| author_facet | Hongguang Fan Litao Li Xiangjian Zhang Ying Liu Chenhui Yang Yi Yang Jing Yin |
| author_sort | Hongguang Fan |
| collection | DOAJ |
| description | Inflammatory damage plays an important role in cerebral ischemic pathogenesis and may represent a target for treatment. Toll-like receptor-4 (TLR4), toll-like receptor-2 (TLR2), myeloid differentiation factor 88 (MyD88), and nuclear factor kappa-B (NF-κB) have been linked to inflammatory reactions. Our previous studies have proved that oxymatrine (OMT) protected ischemic brain injury and this effect may be through the decreasing of NF-κB expression. However, little is known regarding the mechanism of OMT in the
acute phase of ischemic stroke. We therefore investigated the
OMT's potential neuroprotective role and the underlying
mechanisms. Male, Sprague-Dawley rats were randomly divided into
sham, saline and OMT treatment groups. We used a middle cerebral
artery occlusion (MCAO) model and administered OMT
intraperitoneally immediately after cerebral ischemia and once
daily on the following days. At time points after MCAO, brain
water content and infarct size were measured. Immunohistochemistry
and RT-PCR were used to analyse the expression of TLR4, TLR2,
MyD88, and NF-κB at gene and protein level in ischemic brain
tissue. The result indicated that OMT protected the brain from
damage caused by MCAO; this effect may be through downregulation
of the TLR4, TLR2, MyD88, and NF-κB. |
| format | Article |
| id | doaj-art-1fe36fba5ff94f67b25104476d049019 |
| institution | OA Journals |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2009-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-1fe36fba5ff94f67b25104476d0490192025-08-20T02:03:47ZengWileyMediators of Inflammation0962-93511466-18612009-01-01200910.1155/2009/704706704706Oxymatrine Downregulates TLR4, TLR2, MyD88, and NF-κB and Protects Rat Brains against Focal IschemiaHongguang Fan0Litao Li1Xiangjian Zhang2Ying Liu3Chenhui Yang4Yi Yang5Jing Yin6Department of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, ChinaDepartment of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, ChinaDepartment of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, ChinaDepartment of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, ChinaDepartment of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, ChinaDepartment of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, ChinaDepartment of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, ChinaInflammatory damage plays an important role in cerebral ischemic pathogenesis and may represent a target for treatment. Toll-like receptor-4 (TLR4), toll-like receptor-2 (TLR2), myeloid differentiation factor 88 (MyD88), and nuclear factor kappa-B (NF-κB) have been linked to inflammatory reactions. Our previous studies have proved that oxymatrine (OMT) protected ischemic brain injury and this effect may be through the decreasing of NF-κB expression. However, little is known regarding the mechanism of OMT in the acute phase of ischemic stroke. We therefore investigated the OMT's potential neuroprotective role and the underlying mechanisms. Male, Sprague-Dawley rats were randomly divided into sham, saline and OMT treatment groups. We used a middle cerebral artery occlusion (MCAO) model and administered OMT intraperitoneally immediately after cerebral ischemia and once daily on the following days. At time points after MCAO, brain water content and infarct size were measured. Immunohistochemistry and RT-PCR were used to analyse the expression of TLR4, TLR2, MyD88, and NF-κB at gene and protein level in ischemic brain tissue. The result indicated that OMT protected the brain from damage caused by MCAO; this effect may be through downregulation of the TLR4, TLR2, MyD88, and NF-κB.http://dx.doi.org/10.1155/2009/704706 |
| spellingShingle | Hongguang Fan Litao Li Xiangjian Zhang Ying Liu Chenhui Yang Yi Yang Jing Yin Oxymatrine Downregulates TLR4, TLR2, MyD88, and NF-κB and Protects Rat Brains against Focal Ischemia Mediators of Inflammation |
| title | Oxymatrine Downregulates TLR4, TLR2, MyD88, and NF-κB and Protects Rat Brains against Focal Ischemia |
| title_full | Oxymatrine Downregulates TLR4, TLR2, MyD88, and NF-κB and Protects Rat Brains against Focal Ischemia |
| title_fullStr | Oxymatrine Downregulates TLR4, TLR2, MyD88, and NF-κB and Protects Rat Brains against Focal Ischemia |
| title_full_unstemmed | Oxymatrine Downregulates TLR4, TLR2, MyD88, and NF-κB and Protects Rat Brains against Focal Ischemia |
| title_short | Oxymatrine Downregulates TLR4, TLR2, MyD88, and NF-κB and Protects Rat Brains against Focal Ischemia |
| title_sort | oxymatrine downregulates tlr4 tlr2 myd88 and nf κb and protects rat brains against focal ischemia |
| url | http://dx.doi.org/10.1155/2009/704706 |
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