Effects of progesterone on the inflammatory response to brain injury in the rat

Traumatic brain injury (TBI) can induce a persistent inflammatory response, histopathological changes and apoptosis in the intestine. Glutamine has been shown to reduce bacterial translocation and maintain intestine mucosal integrity, but its effects on the inflammatory response, structural alterations and apoptosis in intestinal mucosa following TBI have not been previously investigated. Using the weight-drop method, a right parietal cortical contusion was induced in rats and, for the next 5 days, they were fed either chow alone or chow mixed with glutamine. Intestinal tissue samples were then removed for analysis. Following TBI, glutamine supplementation was found to: decrease intestinal concentrations of interleukin (IL) −1β, tumour necrosis factor-α (TNF-α) and IL-6; downregulate intercellular adhesion molecule-1 (ICAM-1) expression; attenuate TBI-induced damage to the intestine structure; and reduce apoptosis. These results suggest that post-TBI glutamine administration could suppress intestinal inflammation, protect intestinal mucosal structure and reduce mucosal apoptosis.

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Omega-3 polyunsaturated fatty acid attenuates the inflammatory response by modulating microglia polarization through SIRT1-mediated deacetylation of the HMGB1/NF-κB pathway following experimental traumatic brain injury

Journal of Neuroinflammation ◽

10.1186/s12974-018-1151-3 ◽

2018 ◽

Vol 15 (1) ◽

Cited By ~ 43

Author(s):

Xiangrong Chen ◽

Chunnuan Chen ◽

Sining Fan ◽

Shukai Wu ◽

Fuxing Yang ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Fatty Acid ◽

Brain Injury ◽

Inflammatory Response ◽

Polyunsaturated Fatty Acid ◽

Omega 3 ◽

Microglia Polarization ◽

Experimental Traumatic Brain Injury

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Annexin A2 Deficiency Exacerbates Neuroinflammation and Long-Term Neurological Deficits after Traumatic Brain Injury in Mice

International Journal of Molecular Sciences ◽

10.3390/ijms20246125 ◽

2019 ◽

Vol 20 (24) ◽

pp. 6125 ◽

Cited By ~ 5

Author(s):

Ning Liu ◽

Yinghua Jiang ◽

Joon Yong Chung ◽

Yadan Li ◽

Zhanyang Yu ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Inflammatory Response ◽

Neurovascular Unit ◽

Annexin A2 ◽

Tissue Loss ◽

Neurological Deficits ◽

Endogenous Factors ◽

The Brain

Our laboratory and others previously showed that Annexin A2 knockout (A2KO) mice had impaired blood–brain barrier (BBB) development and elevated pro-inflammatory response in macrophages, implying that Annexin A2 (AnxA2) might be one of the key endogenous factors for maintaining homeostasis of the neurovascular unit in the brain. Traumatic brain injury (TBI) is an important cause of disability and mortality worldwide, and neurovascular inflammation plays an important role in the TBI pathophysiology. In the present study, we aimed to test the hypothesis that A2KO promotes pro-inflammatory response in the brain and worsens neurobehavioral outcomes after TBI. TBI was conducted by a controlled cortical impact (CCI) device in mice. Our experimental results showed AnxA2 expression was significantly up-regulated in response to TBI at day three post-TBI. We also found more production of pro-inflammatory cytokines in the A2KO mouse brain, while there was a significant increase of inflammatory adhesion molecules mRNA expression in isolated cerebral micro-vessels of A2KO mice compared with wild-type (WT) mice. Consistently, the A2KO mice brains had a significant increase in leukocyte brain infiltration at two days after TBI. Importantly, A2KO mice had significantly worse sensorimotor and cognitive function deficits up to 28 days after TBI and significantly larger brain tissue loss. Therefore, these results suggested that AnxA2 deficiency results in exacerbated early neurovascular pro-inflammation, which leads to a worse long-term neurologic outcome after TBI.

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Ibuprofen attenuates the inflammatory response and allows formation of migratory neuroblasts from grafted stem cells after traumatic brain injury

Restorative Neurology and Neuroscience ◽

10.3233/rnn-2011-0606 ◽

2012 ◽

Vol 30 (1) ◽

pp. 9-19 ◽

Cited By ~ 2

Author(s):

U. Wallenquist ◽

K. Holmqvist ◽

A. Hånell ◽

N. Marklund ◽

L. Hillered ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Stem Cells ◽

Brain Injury ◽

Inflammatory Response

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Severe Traumatic Brain Injury (TBI) Modulates the Kinetic Profile of the Inflammatory Response of Markers for Neuronal Damage

Journal of Clinical Medicine ◽

10.3390/jcm9061667 ◽

2020 ◽

Vol 9 (6) ◽

pp. 1667 ◽

Cited By ~ 3

Author(s):

Cora Rebecca Schindler ◽

Thomas Lustenberger ◽

Mathias Woschek ◽

Philipp Störmann ◽

Dirk Henrich ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Inflammatory Response ◽

Calcium Binding ◽

Injury Severity ◽

Neuronal Damage ◽

Severe Trauma ◽

Multiple Injuries ◽

Kinetic Profile ◽

Severe Tbi

The inflammatory response plays an important role in the pathophysiology of multiple injuries. This study examines the effects of severe trauma and inflammatory response on markers of neuronal damage. A retrospective analysis of prospectively collected data in 445 trauma patients (Injury Severity Score (ISS) ≥ 16) is provided. Levels of neuronal biomarkers (calcium-binding Protein B (S100b), Enolase2 (NSE), glial fibrillary acidic protein (GFAP)) and Interleukins (IL-6, IL-10) in severely injured patients (with polytrauma (PT)) without traumatic brain injury (TBI) or with severe TBI (PT+TBI) and patients with isolated TBI (isTBI) were measured upon arrival until day 5. S100b, NSE, GFAP levels showed a time-dependent decrease in all cohorts. Their expression was higher after multiple injuries (p = 0.038) comparing isTBI. Positive correlation of marker level after concomitant TBI and isTBI (p = 0.001) was noted, while marker expression after PT appears to be independent. Highest levels of IL-6 and -10 were associated to PT und lowest to isTBI (p < 0.001). In all groups pro-inflammatory response (IL-6/-10 ratio) peaked on day 2 and at a lower level on day 4. Severe TBI modulates kinetic profile of inflammatory response by reducing interleukin expression following trauma. Potential markers for neuronal damage have a limited diagnostic value after severe trauma because undifferentiated increase.

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Effect of systemic LPS injection on cortical NF-κB activity and inflammatory response following traumatic brain injury in rats

Brain Research ◽

10.1016/j.brainres.2004.07.090 ◽

2004 ◽

Vol 1026 (1) ◽

pp. 23-32 ◽

Cited By ~ 75

Author(s):

Chun-hua Hang ◽

Ji-xin Shi ◽

Jie Tian ◽

Jie-shou Li ◽

Wei Wu ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Inflammatory Response

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Inhibiting HMGB1 with Glycyrrhizic Acid Protects Brain Injury after DAI via Its Anti-Inflammatory Effect

Mediators of Inflammation ◽

10.1155/2016/4569521 ◽

2016 ◽

Vol 2016 ◽

pp. 1-9 ◽

Cited By ~ 23

Author(s):

Honggang Pang ◽

Tinqin Huang ◽

Jinning Song ◽

Dandong Li ◽

Yonglin Zhao ◽

...

Keyword(s):

Brain Injury ◽

Inflammatory Response ◽

Proinflammatory Cytokines ◽

Neuronal Apoptosis ◽

Glycyrrhizic Acid ◽

Axonal Injury ◽

Tunel Staining ◽

Hmgb1 Level ◽

Associated Proteins ◽

The Brain

High-mobility group box 1 (HMGB1), a nuclear protein that has endogenous cytokine-like activity, is involved in several neurological diseases by mediating inflammatory response. In this study, a lateral head rotation device was used to establish a rat diffuse axonal injury (DAI) model. The dynamic expression of HMGB1, apoptosis-associated proteins, and proinflammatory cytokines were detected by Western blot, and neuronal apoptosis was observed by TUNEL staining. The extracellular release of HMGB1 and the accumulation ofβ-APP were observed by immunofluorescence and immunohistochemistry, respectively. The brain injury was indicated by modified neurological severity score (mNSS), brain water content (BWC), and the extravasation of Evans blue. We showed that HMGB1 level obviously decreased within 48 h after DAI, accompanied by neuronal apoptosis, the activation of caspases 3 and 9, and the phosphorylation of BCL-2. Inhibiting HMGB1 with glycyrrhizic acid (GL) can suppress the activation of apoptosis-associated proteins and inhibit the expression of proinflammatory cytokines, which ameliorated motor and cognitive deficits, reduced neuronal apoptosis, and protected the integrity of blood brain barrier (BBB) and axonal injury after experimental DAI in rats. Thus, HMGB1 may be involved in the inflammatory response after DAI, and inhibition of HMGB1 release with GL can notably alleviate the brain injury after DAI.

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