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PMC:2817507 / 12025-18287 JSONTXT 26 Projects

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Id Subject Object Predicate Lexical cue
T125 0-2 Sentence denotes 4.
T126 3-13 Sentence denotes Discussion
T6193 14-188 Sentence denotes Intra-cerebral hemorrhage (ICH) represents 10–15% of all strokes, and occurs with increasing frequency as a complication of the thrombolytic treatment of ischemic stroke [1].
T127 14-188 Sentence denotes Intra-cerebral hemorrhage (ICH) represents 10–15% of all strokes, and occurs with increasing frequency as a complication of the thrombolytic treatment of ischemic stroke [1].
T6194 189-249 Sentence denotes The mortality of ICH is higher than that of ischemic stroke.
T128 189-249 Sentence denotes The mortality of ICH is higher than that of ischemic stroke.
T6195 250-300 Sentence denotes Only 31% are functionally independent at 3 months.
T129 250-300 Sentence denotes Only 31% are functionally independent at 3 months.
T6196 301-352 Sentence denotes Only 38% of the patients survive the 1st year [10].
T130 301-352 Sentence denotes Only 38% of the patients survive the 1st year [10].
T6197 353-472 Sentence denotes Unfortunately, the method for treatment of this disease and protection of the brain tissue after ICH are not effective.
T131 353-472 Sentence denotes Unfortunately, the method for treatment of this disease and protection of the brain tissue after ICH are not effective.
T6198 473-566 Sentence denotes Mass effect, ischemia, and toxicity of blood components after ICH induce brain tissue damage.
T132 473-566 Sentence denotes Mass effect, ischemia, and toxicity of blood components after ICH induce brain tissue damage.
T6199 567-676 Sentence denotes In addition, there is increasing evidence that inflammatory processes are involved in cerebrovascular events.
T133 567-676 Sentence denotes In addition, there is increasing evidence that inflammatory processes are involved in cerebrovascular events.
T6200 677-870 Sentence denotes After ICH, inflammatory mediators from the blood might enter to the brain and induce an inflammatory reaction and the brain cells itself are also capable of producing many of these agents [11].
T134 677-870 Sentence denotes After ICH, inflammatory mediators from the blood might enter to the brain and induce an inflammatory reaction and the brain cells itself are also capable of producing many of these agents [11].
T6201 871-1000 Sentence denotes The inflammatory responses are responsible for the ICH induced brain injury, which could provide new therapeutic targets for ICH.
T135 871-1000 Sentence denotes The inflammatory responses are responsible for the ICH induced brain injury, which could provide new therapeutic targets for ICH.
T6202 1001-1182 Sentence denotes Various constituents of the inflammatory response, including adhesion molecules, cytokines, leukocytes, immunoglobulins, and complement, may be important in the pathogenesis of ICH.
T136 1001-1182 Sentence denotes Various constituents of the inflammatory response, including adhesion molecules, cytokines, leukocytes, immunoglobulins, and complement, may be important in the pathogenesis of ICH.
T6203 1183-1291 Sentence denotes However, how the inflammatory responses is activated and regulated in the brain tissue after ICH is unclear.
T137 1183-1291 Sentence denotes However, how the inflammatory responses is activated and regulated in the brain tissue after ICH is unclear.
T6204 1292-1561 Sentence denotes Transcription factor nuclear factor-kappa-B (NFκB) is an important nuclear transcription factor, which initiates transcription of genes associated with immune responses and inflammation [12, 13] and also plays a key role in regulating inflammation in brain pathologies.
T138 1292-1561 Sentence denotes Transcription factor nuclear factor-kappa-B (NFκB) is an important nuclear transcription factor, which initiates transcription of genes associated with immune responses and inflammation [12, 13] and also plays a key role in regulating inflammation in brain pathologies.
T6205 1562-1648 Sentence denotes It has been reported that NFκB increased in the region of perihematoma after ICH [14].
T139 1562-1648 Sentence denotes It has been reported that NFκB increased in the region of perihematoma after ICH [14].
T6206 1649-1810 Sentence denotes NFκB activation occurs within minutes and persists for at least a week in response to ICH, which is associated with the expression of selected target genes [15].
T140 1649-1810 Sentence denotes NFκB activation occurs within minutes and persists for at least a week in response to ICH, which is associated with the expression of selected target genes [15].
T6207 1811-1941 Sentence denotes Activation of NFκB initiates inflammatory responses and contributes to the pathobiology of perilesional cell death after ICH [16].
T141 1811-1941 Sentence denotes Activation of NFκB initiates inflammatory responses and contributes to the pathobiology of perilesional cell death after ICH [16].
T6208 1942-2129 Sentence denotes Inhibition of NFκB activity has been shown to have a therapeutic effect on experimental ICH, such as reduce inflammation, behavioral dysfunction, and neuronal damage produced by ICH [17].
T142 1942-2129 Sentence denotes Inhibition of NFκB activity has been shown to have a therapeutic effect on experimental ICH, such as reduce inflammation, behavioral dysfunction, and neuronal damage produced by ICH [17].
T6209 2130-2263 Sentence denotes The knowledge about how NFκB is activated in the brain subjected to ICH is critical for seeking a new neuroprotective method for ICH.
T143 2130-2263 Sentence denotes The knowledge about how NFκB is activated in the brain subjected to ICH is critical for seeking a new neuroprotective method for ICH.
T6210 2264-2415 Sentence denotes Toll-like receptors (TLRs) are a family of signal transduction molecules and play a critical role in the induction of innate and adaptive immunity [4].
T144 2264-2415 Sentence denotes Toll-like receptors (TLRs) are a family of signal transduction molecules and play a critical role in the induction of innate and adaptive immunity [4].
T6211 2416-2497 Sentence denotes TLR-mediated signaling pathways mainly stimulate the activation of NFκB [12, 13].
T145 2416-2497 Sentence denotes TLR-mediated signaling pathways mainly stimulate the activation of NFκB [12, 13].
T6212 2498-2707 Sentence denotes TLR4, the first mammalian TLR recognized, has been reported to be involved in several central nervous (CNS) system diseases, such as inflammatory or autoimmune CNS diseases and cerebral ischemic injury [7, 8].
T146 2498-2707 Sentence denotes TLR4, the first mammalian TLR recognized, has been reported to be involved in several central nervous (CNS) system diseases, such as inflammatory or autoimmune CNS diseases and cerebral ischemic injury [7, 8].
T6213 2708-3030 Sentence denotes Although previous reports indicated that the activation of NFκB was attributed to the oxidative stress or glutamate receptor activation induced by red blood cells and/or plasma constituents [17], very few studies have been directed to investigate the role and the relationship between TLR4-mediated NFκB signaling and ICH.
T147 2708-3030 Sentence denotes Although previous reports indicated that the activation of NFκB was attributed to the oxidative stress or glutamate receptor activation induced by red blood cells and/or plasma constituents [17], very few studies have been directed to investigate the role and the relationship between TLR4-mediated NFκB signaling and ICH.
T6214 3031-3141 Sentence denotes In the present study, we established the rat model of experimental ICH and detected the TLR4 mRNA and protein.
T148 3031-3141 Sentence denotes In the present study, we established the rat model of experimental ICH and detected the TLR4 mRNA and protein.
T6215 3142-3276 Sentence denotes Our data showed that transcription of TLR4 as well as the expression of TLR4 protein after ICH significantly elevated in brain tissue.
T149 3142-3276 Sentence denotes Our data showed that transcription of TLR4 as well as the expression of TLR4 protein after ICH significantly elevated in brain tissue.
T6216 3277-3392 Sentence denotes These changes started as early as 6 hours after the ICH insult and maintained at a high level for 7 days afterward.
T150 3277-3392 Sentence denotes These changes started as early as 6 hours after the ICH insult and maintained at a high level for 7 days afterward.
T6217 3393-3571 Sentence denotes The TLR4 protein, detected by immunohistochemistry, was consistently distributed in peri-hemorrhage areas, the hippocampus, cortex, thalamic nuclei, and some white matter tracts.
T151 3393-3571 Sentence denotes The TLR4 protein, detected by immunohistochemistry, was consistently distributed in peri-hemorrhage areas, the hippocampus, cortex, thalamic nuclei, and some white matter tracts.
T6218 3572-3720 Sentence denotes These data indicated that increased expression of TLR4 may be related to the triggering of the inflammatory responses in the brain tissue after ICH.
T152 3572-3720 Sentence denotes These data indicated that increased expression of TLR4 may be related to the triggering of the inflammatory responses in the brain tissue after ICH.
T6219 3721-3869 Sentence denotes Recent studies demonstrated that ICH initiates inflammatory responses, which are associated with secondary growth of hemorrhage and cell death [18].
T153 3721-3869 Sentence denotes Recent studies demonstrated that ICH initiates inflammatory responses, which are associated with secondary growth of hemorrhage and cell death [18].
T6220 3870-3986 Sentence denotes It is now believed that TLR4-mediated-NFκB pathway activates and regulates immunological and inflammatory responses.
T154 3870-3986 Sentence denotes It is now believed that TLR4-mediated-NFκB pathway activates and regulates immunological and inflammatory responses.
T6221 3987-4241 Sentence denotes To investigate the mechanisms underlying the increased inflammatory responses in the brain after ICH, in the present study, we evaluated the activation of TLR4-mediated NFκB signaling by detecting the p-IκB and the activity of NFκB in hemorrhagic brains.
T155 3987-4241 Sentence denotes To investigate the mechanisms underlying the increased inflammatory responses in the brain after ICH, in the present study, we evaluated the activation of TLR4-mediated NFκB signaling by detecting the p-IκB and the activity of NFκB in hemorrhagic brains.
T6222 4242-4334 Sentence denotes NFκB is an important transcription factor downstream in the TLR4-mediated signaling pathway.
T156 4242-4334 Sentence denotes NFκB is an important transcription factor downstream in the TLR4-mediated signaling pathway.
T6223 4335-4550 Sentence denotes Activation of TLR4 stimulates IκBα phosphorylation and degradation, resulting in nuclear translocation of NFκB, which initiates transcription of genes associated with innate immune responses and inflammation [5, 6].
T157 4335-4550 Sentence denotes Activation of TLR4 stimulates IκBα phosphorylation and degradation, resulting in nuclear translocation of NFκB, which initiates transcription of genes associated with innate immune responses and inflammation [5, 6].
T6224 4551-4685 Sentence denotes We observed that the levels of phosphorylation of IκB and the activity of NFκB were significantly increased in brain tissue after ICH.
T158 4551-4685 Sentence denotes We observed that the levels of phosphorylation of IκB and the activity of NFκB were significantly increased in brain tissue after ICH.
T6225 4686-4807 Sentence denotes The temporal profile of the expression of p-IκB and the activation of NFκB was similar to that of the expression of TLR4.
T159 4686-4807 Sentence denotes The temporal profile of the expression of p-IκB and the activation of NFκB was similar to that of the expression of TLR4.
T6226 4808-5015 Sentence denotes Our data suggest that ICH stimulates activation of the TLR4/NFκB signaling pathway, which is consistent with previous reports that activation of NFκB is regulated through the TLR4-mediated signaling pathway.
T160 4808-5015 Sentence denotes Our data suggest that ICH stimulates activation of the TLR4/NFκB signaling pathway, which is consistent with previous reports that activation of NFκB is regulated through the TLR4-mediated signaling pathway.
T6227 5016-5328 Sentence denotes TLR4 plays an important role in the recognition of microbial components [19, 20] and can also recognize endogenous molecules such as the degradation products of macromolecules, products of proteolytic cascades, intracellular components of ruptured cells, and products of genes that are activated by inflammation.
T161 5016-5328 Sentence denotes TLR4 plays an important role in the recognition of microbial components [19, 20] and can also recognize endogenous molecules such as the degradation products of macromolecules, products of proteolytic cascades, intracellular components of ruptured cells, and products of genes that are activated by inflammation.
T6228 5329-5525 Sentence denotes For instance, HSP70, HSP32, HSP27, and enzymes involved in oxidative stress are found to be upregulated in the brain after ICH, which may be produced by injured neuronal cells or blood cells [21].
T162 5329-5525 Sentence denotes For instance, HSP70, HSP32, HSP27, and enzymes involved in oxidative stress are found to be upregulated in the brain after ICH, which may be produced by injured neuronal cells or blood cells [21].
T6229 5526-5773 Sentence denotes It may be speculated that these molecules produced in damaged brain or came from blood cells and constituents of plasma server as endogenous TLR4 ligands, activate TLR4-mediated NFκB signaling, and initiate the inflammatory responses in IHC brain.
T163 5526-5773 Sentence denotes It may be speculated that these molecules produced in damaged brain or came from blood cells and constituents of plasma server as endogenous TLR4 ligands, activate TLR4-mediated NFκB signaling, and initiate the inflammatory responses in IHC brain.
T6230 5774-5921 Sentence denotes However, the specific endogenous ligands for TLR4 in hemorrhagic brain have not been determined and need to be identified through further research.
T164 5774-5921 Sentence denotes However, the specific endogenous ligands for TLR4 in hemorrhagic brain have not been determined and need to be identified through further research.
T6231 5922-6262 Sentence denotes In conclusion, the present study demonstrated the temporal profile of the activation of TLR4-mediated NFκB signaling in brain tissue in a rat model of experimental ICH, which suggests that TLR4-mediated NFκB signaling participates in the pathogenesis of ICH, which may be a therapeutic target for the prevention of ICH-induced brain damage.
T165 5922-6262 Sentence denotes In conclusion, the present study demonstrated the temporal profile of the activation of TLR4-mediated NFκB signaling in brain tissue in a rat model of experimental ICH, which suggests that TLR4-mediated NFκB signaling participates in the pathogenesis of ICH, which may be a therapeutic target for the prevention of ICH-induced brain damage.