scholarly journals Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2) Mediates Neuroprotection in Traumatic Brain Injury at Least in Part by Inactivating Microglia

2016 ◽  
Vol 22 ◽  
pp. 2161-2166 ◽  
Author(s):  
Gang Wu ◽  
Zongying Liu
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Related Factor ◽  
Nuclear Factor

Cinnamon Polyphenol Extract Exerts Neuroprotective Activity in Traumatic Brain Injury in Male Mice

2018 ◽  
Vol 17 (6) ◽  
pp. 439-447 ◽  
Author(s):  
Burak Yulug ◽  
Ertugrul Kilic ◽  
Serdar Altunay ◽  
Cenk Ersavas ◽  
Cemal Orhan ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Signaling Pathways ◽  
Intraperitoneal Administration ◽  
Neuroprotective Activity ◽  
Vehicle Group ◽  
Related Factor ◽  
Nuclear Factor ◽  
Male Mice

Background: Cinnamon polyphenol extract is a traditional spice commonly used in different areas of the world for the treatment of different disease conditions which are associated with inflammation and oxidative stress. Despite many preclinical studies showing the anti-oxidative and antiinflammatory effects of cinnamon, the underlying mechanisms in signaling pathways via which cinnamon protects the brain after brain trauma remained largely unknown. However, there is still no preclinical study delineating the possible molecular mechanism of neuroprotective effects cinnamon polyphenol extract in Traumatic Brain Injury (TBI). The primary aim of the current study was to test the hypothesis that cinnamon polyphenol extract administration would improve the histopathological outcomes and exert neuroprotective activity through its antioxidative and anti-inflammatory properties following TBI. Methods: To investigate the effects of cinnamon, we induced brain injury using a cold trauma model in male mice that were treated with cinnamon polyphenol extract (10 mg/kg) or vehicle via intraperitoneal administration just after TBI. Mice were divided into two groups: TBI+vehicle group and TBI+ cinnamon polyphenol extract group. Brain samples were collected 24 h later for analysis. Results: We have shown that cinnamon polyphenol extract effectively reduced infarct and edema formation which were associated with significant alterations in inflammatory and oxidative parameters, including nuclear factor-κB, interleukin 1-beta, interleukin 6, nuclear factor erythroid 2-related factor 2, glial fibrillary acidic protein, neural cell adhesion molecule, malondialdehyde, superoxide dismutase, catalase and glutathione peroxidase. Conclusion: Our results identify an important neuroprotective role of cinnamon polyphenol extract in TBI which is mediated by its capability to suppress the inflammation and oxidative injury. Further, specially designed experimental studies to understand the molecular cross-talk between signaling pathways would provide valuable evidence for the therapeutic role of cinnamon in TBI and other TBI related conditions.

Expression of nuclear factor erythroid 2-related factor 2 following traumatic brain injury in the human brain

Neuroreport ◽  
2019 ◽  
Vol 30 (5) ◽  
pp. 344-349 ◽  
Author(s):  
Yuxin He ◽  
Huiying Yan ◽  
Hongbin Ni ◽  
Weibang Liang ◽  
Wei Jin
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Human Brain ◽  
Related Factor ◽  
Nuclear Factor

scholarly journals Curcumin Plays Neuroprotection Activity by Modulation of Neurotrophic Factor BDNF, GAP-43 and GFAP in Mice with Traumatic Brain Injury (P06-043-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Nurhan Sahin ◽  
Ertugrul Kilic ◽  
Nilay Ates ◽  
Zeynep Balcikanli ◽  
Cemal Orhan ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neurotrophic Factor ◽  
Infarct Volume ◽  
Intraperitoneal Administration ◽  
Vehicle Group ◽  
Related Factor ◽  
Nuclear Factor ◽  
Health Technologies ◽  
The Brain

Abstract Objectives Curcumin, extracted from the rhizome Curcuma longa, has been shown to be beneficial for neuroprotection in previous studies. In a recent study, a novel formulation of curcumin resulted in an increased relative absorption by 46 times (CurcuWIN®) of the total curcuminoids over the unformulated standard curcumin form. However, the exact mechanisms by which curcumin demonstrates its neuroprotective effects are not fully understood. The present study aimed to investigate the effects of curcumin supplementation on the expression of brain-derived neurotrophic factor (BDNF), glial fibrillary acidic protein (GFAP), a main component of the glial scar, and growth-associated protein-43 (GAP-43), a signaling molecule in traumatic brain injury (TBI). Methods Brain injury was induced using a cold trauma model in male mice that were treated with curcumin (50 mg/kg) or vehicle via intraperitoneal administration just after TBI. Mice were divided into two groups: TBI + vehicle group and TBI + curcumin (CurcuWIN) group. Results The results show that curcumin treatment reduced the infarct volume in the brain. TBI induction increased inflammatory cytokines (IL-1β and IL-6), nuclear factor-κB (NF-κB) and GFAP, and reduced BDNF, GAP-43, neural cell adhesion molecule (ICAM) and nuclear factor erythroid 2-related factor 2 (Nrf2) levels in the brain. Interestingly, curcumin decreased the levels of NF-κB, IL-1β, IL-6, and GFAP, and increased BDNF, GAP-43, ICAM and Nrf2 levels in the brain. Conclusions In conclusion, these results showed that curcumin could increase the levels of BDNF, GAP-43, ICAM, and Nrf2 and attenuate brain injury in the model of TBI. Funding Sources This study was supported by OmniActive Health Technologies Inc. (NJ, USA). This work was also supported in part by the Turkish Academy of Sciences. Supporting Tables, Images and/or Graphs

scholarly journals Effects of Tert-Butylhydroquinone on Intestinal Inflammatory Response and Apoptosis following Traumatic Brain Injury in Mice

2010 ◽  
Vol 2010 ◽  
pp. 1-7 ◽  
Author(s):  
Wei Jin ◽  
Hongbin Ni ◽  
Yuxiang Dai ◽  
Handong Wang ◽  
Tianyu Lu ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Inflammatory Response ◽  
Intestinal Inflammation ◽  
Closed Head Injury ◽  
Mucosal Injury ◽  
Intercellular Adhesion Molecule ◽  
Vehicle Group ◽  
Related Factor ◽  
Nuclear Factor

Traumatic brain injury (TBI) can induce intestinal inflammatory response and mucosal injury. Antioxidant transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) has been shown in our previous studies to prevent oxidative stress and inflammatory response in gut after TBI. The objective of this study was to test whether tert-butylhydroquinone (tBHQ), an Nrf2 inducer, can protect against TBI-induced intestinal inflammatory response and mucosal injury in mice. Adult male ICR mice were randomly divided into three groups: (1) sham + vehicle group, (2) TBI + vehicle group, and (3) TBI + tBHQ group (n=12per group). Closed head injury was adopted using Hall's weight-dropping method. Intestinal mucosa apoptosis and inflammatory-related factors, such as nuclear factor kappa B (NF-κB), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6) and intercellular adhesion molecule-1 (ICAM-1), were investigated at 24 h after TBI. As a result, we found that oral treatment with 1% tBHQ prior to TBI for one week markedly decreased NF-κB activation, inflammatory cytokines production, and ICAM-1 expression in the gut. Administration of tBHQ also significantly attenuated TBI-induced intestinal mucosal apoptosis. The results of the present study suggest that tBHQ administration could suppress the intestinal inflammation and reduce the mucosal damage following TBI.

scholarly journals Efficacy of Minocycline in Neural Stem Cells Proliferation after Traumatic Brain Injury

2020 ◽  
Vol 8 (A) ◽  
pp. 59-64
Author(s):  
R. R. Suzy Indharty ◽  
Iskandar Japardi ◽  
Andre M. P. Siahaan ◽  
Steven Tandean ◽  
Michael Lumintang Loe
Keyword(s):  
Traumatic Brain Injury ◽  
Stem Cells ◽  
Brain Injury ◽  
Neural Stem Cells ◽  
Inflammatory Responses ◽  
Closed Head Injury ◽  
Related Factor ◽  
Sprague Dawley ◽  
Proliferation Capacity ◽  
Cell Counts

BACKGROUND: Neuroinflammation is an important secondary injury mechanism that contributes to neurological impairments after traumatic brain injury (TBI). There is a robust evidence that neuroinflammation will diminish neurogenesis after TBI. Therefore, strategies to attenuate the inflammatory responses are potential to increase neurogenesis following TBI. Minocycline, a second-generation tetracycline antibiotic derivate, has potent anti-inflammatory effect by reducing microglial activation and suppressing some pro-inflammatory cytokines. AIM: The aim of this study is to investigate if minocycline could enhance neurogenesis after TBI. METHODS: Thirty Sprague Dawley rats were randomized into three treatments group, i.e., sham-operated controls, closed head injury (CHI), and CHI with minocycline. We used the modified Feeney’s weight-drop model for making CHI. For the treatment group, we gave minocycline per oral (50 mg/kg) twice daily for the first 2 days followed by 25 mg/kg once daily for 3 consecutive days. Animals were sacrificed on day 5. To assess the proliferation capacity of neural stem cells (NSC), we performed immunohistochemistry staining with SOX2, brain-derived neurotropic factor (BDNF), and NFR. Cell counts were carried out using light microscope with 1000 times magnification in 20 high-power fields. RESULTS: SOX2, NF-E2-related factor 2 (NRF-2), and BDNF were upregulated in the CHI group compared to the sham-operated group (p < 0.05). NRF-2, BDNF, and SOX2 were upregulated also significantly in the CHI+ minocycline group compared to the sham-operated group and the CHI group (p < 0.05). CONCLUSION: Minocycline increased the proliferation capacity of NSC.

scholarly journals Aucubin alleviates oxidative stress and inflammation via Nrf2-mediated signaling activity in experimental traumatic brain injury

2020 ◽  
Author(s):  
Han Wang ◽  
Xiaoming Zhou ◽  
Lingyun Wu ◽  
Guangjie Liu ◽  
Weidong Xu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cortical Neurons ◽  
Neurological Deficits ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tunel Staining ◽  
Related Factor ◽  
Mice Model ◽  
Anti Inflammatory

Abstract Background: Aucubin (Au) has anti-oxidative and anti-inflammatory bioactivities; however, its effects on a traumatic brain injury (TBI) model remain unknown. We explored the potential role of Au in a H2O2-induced oxidant damage in primary cortical neurons and weight-drop induced-TBI in a mouse model.Methods: Neuronal apoptosis, brain water content, histological damages and neurological deficits and cognitive functions were measured. We performed western blot, TdT-mediated dUTP Nick-End Labeling (TUNEL) staining, Nissl staining, quantitative real time polymerase chain reaction (q-PCR), immunofluorescence/immunohistochemistry and enzyme linked immunosorbent assay (ELISA). RNA interference experiments were performed to determine the effects of Nuclear factor erythroid-2 related factor 2 (Nrf2) on TBI mice with intraperitoneal injection of Au.Results: We found that Au enhanced the translocation of Nrf2 into the nucleus, activated antioxidant enzymes, suppressed excessive generation of reactive oxygen species (ROS) and reduced cell apoptosis in vitro and vivo experiments. In the mice model of TBI, Au markedly attenuated brain edema, histological damages and improved neurological and cognitive deficits. Au significantly suppressed high mobility group box 1(HMGB1)-mediated aseptic inflammation. Nrf2 knockdown in TBI mice blunted the antioxidant and anti-inflammatory neuroprotective effects of the Au.Conclusions: Taken together, our data suggest that Au provides a neuroprotective effect in TBI mice model by inhibiting oxidative stress and inflammatory responses; the mechanisms involve triggering Nrf2-induced antioxidant system.

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