scholarly journals Neuroprotective effects of crude extract of Crataegus songarica on a rat model of traumatic brain injury

2022 ◽  
Vol 20 (2) ◽  
pp. 293-299
Author(s):  
Xueliang Gao ◽  
Zhao Wang ◽  
Peilei Jia ◽  
Yapeng Zhao ◽  
Kai Wang ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Rat Model ◽  
Brain Cortex ◽  
Neuronal Survival ◽  
Underlying Mechanism ◽  
Tunel Staining ◽  
Heme Oxygenase 1 ◽  
Nissl Staining ◽  
Neuroprotective Effects

Purpose: To investigate the protective effect of Crataegus songarica extract (CSCE) against traumatic brain injury (TBI) in rats, and the underlying mechanism of action. Methods: A rat model of TBI was established via tracheal intubation procedure, and the rats were treated with graded doses of CSCE. Neuronal survival was determined by Nissl staining, while neuronal apoptosis was measured using TUNEL-staining. Neurological impairments were determined based on neurological severity score (NSS). Results: Treatment of TBI rats with CSCE enhanced neuronal survival and decreased TUNEL-positive cell fraction in the brain cortex. The treatment prevented elevation of NSS and suppressed mRNA and protein expression levels of IL-6 and TNF-α in brain cortex. Moreover, CSCE treatment prevented TBI-mediated suppression of activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx), and attenuated hydrogen peroxide (H2O2) levels in TBI rat brain cortex. Treatment of TBI rats with CSCE down-regulated NF-κB expression, increased Nrf2 expression and up-regulated mRNA expressions of heme oxygenase 1 (HO-1) and quinine oxidoreductase 1 (NQO-1). Conclusion: These results suggest that CSCE prevents TBI-mediated reduction in neuronal survival and inhibits brain cortical neuronal death in rats. It improves NSS and inhibits inflammatory response via activation of Nrf2 pathway and targeting of NF-κB expression. Therefore, CSCE is a potential therapeutic agent for TBI.

Estrogen Receptor-α is Involved in Tamoxifen Neuroprotective Effects in a Traumatic Brain Injury Male Rat Model

2018 ◽  
Vol 112 ◽  
pp. e278-e287 ◽  
Author(s):  
Sher-Wei Lim ◽  
Eric Nyam TT ◽  
Cho-Ya Hu ◽  
Chung-Ching Chio ◽  
Che-Chuan Wang ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Estrogen Receptor ◽  
Brain Injury ◽  
Rat Model ◽  
Estrogen Receptor Α ◽  
Male Rat ◽  
Neuroprotective Effects

scholarly journals Neuroprotective effects of food restriction in a rat model of traumatic brain injury – the role of glucocorticoid signaling

2020 ◽  
pp. 1-13
Author(s):  
Milka Perović ◽  
Milena Jović ◽  
Smilja Todorović ◽  
Aleksandra Mladenović Đorđević ◽  
Desanka Milanović ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Rat Model ◽  
Food Restriction ◽  
Neuroprotective Effects ◽  
Glucocorticoid Signaling

scholarly journals S100A8 Promotes Inflammation via Toll-Like Receptor 4 After Experimental Traumatic Brain Injury

2020 ◽  
Author(s):  
Guoyuan He ◽  
Yan-Ling Han ◽  
Degang Wu ◽  
Hao Cheng ◽  
Le-An Sun ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Recombinant Protein ◽  
Underlying Mechanism ◽  
Enzyme Linked Immunosorbent Assay ◽  
Toll Like Receptor ◽  
Nissl Staining ◽  
Neurological Score ◽  
The Brain

Abstract Background: S100A8 is involved in the pathological processes of a variety of central nervous system(CNS) diseases related to inflammation including traumatic brain injury (TBI). However, the underlying mechanism for the induction of inflammation in the brain by S100A8 after TBI remains unclear, which was investigated in the present study.Methods: The weight-drop TBI model was used in this study. The mice were randomly assigned into 5 groups: the Sham, S100A8, S100A8 + TAK-242, TBI, and TBI + TAK-242 groups. In the S100A8 + TAK-242 and TBI + TAK-242 groups, mice were treated with TAK-242, an inhibitor of Toll-like receptor (TLR) 4, intraperitoneally at half an hour before TBI. In the S100A8 and S100A8 + TAK-242 groups, S100A8 recombinant protein was injected into the lateral ventricle of the brain. To explore the relationship between S100A8 and TLR4, Western Blot (WB), immunofluorescence, enzyme-linked immunosorbent assay (ELISA) and Nissl staining were employed. Neurological score and the brain water content were also assessed. Additionally, BV-2 microglial cells were stimulated with lipopolysaccharide (LPS) or S100A8 recombinant protein with/without TAK-242 in vitro. The expressions of the related proteins were subsequently detected with WB or ELISA.Results: The levels of S100A8 protein and pro-inflammatory cytokines were significantly increased after TBI. After intracerebroventricular administration of S100A8, the neurological scores of non-TBI animals were decreased remarkably with severe brain edema. Furthermore, the levels of TLR4, p-p65 and myeloid differentiation factor 88(MyD88) were all increased after S100A8 administration or TBI, which could be restored by TAK-242. Meanwhile, p-p65 and MyD88 were upregulated after S100A8 or LPS stimulation in vitro, which also could be suppressed by TAK-242.Conclusions: The present study demonstrated that TLR4-MyD88 pathway was activated by S100A8, which was essential to the development of inflammation in the brain after TBI.

Neuroprotective Effects of Thymoquinone on the Hippocampus in a Rat Model of Traumatic Brain Injury

2016 ◽  
Vol 86 ◽  
pp. 243-249 ◽  
Author(s):  
İsmail Gülşen ◽  
Hakan Ak ◽  
Neşe Çölçimen ◽  
Hamit H. Alp ◽  
Mehmet E. Akyol ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Rat Model ◽  
Neuroprotective Effects

scholarly journals Normobaric Oxygen Worsens Outcome after a Moderate Traumatic Brain Injury

2015 ◽  
Vol 35 (7) ◽  
pp. 1137-1144 ◽  
Author(s):  
Lora Talley Watts ◽  
Justin Alexander Long ◽  
Venkata Hemanth Manga ◽  
Shiliang Huang ◽  
Qiang Shen ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Lesion Volume ◽  
Nissl Staining ◽  
Neuroprotective Effects ◽  
Normobaric Oxygen ◽  
Moderate Traumatic Brain Injury ◽  
Mri Scans ◽  
Behavioral Assessments ◽  
Double Blinded

Traumatic brain injury (TBI) is a multifaceted injury and a leading cause of death in children, young adults, and increasingly in Veterans. However, there are no neuroprotective agents clinically available to counteract damage or promote repair after brain trauma. This study investigated the neuroprotective effects of normobaric oxygen (NBO) after a controlled cortical impact in rats. The central hypothesis was that NBO treatment would reduce lesion volume and functional deficits compared with air-treated animals after TBI by increasing brain oxygenation thereby minimizing ischemic injury. In a randomized double-blinded design, animals received either NBO ( n = 8) or normal air ( n = 8) after TBI. Magnetic resonance imaging (MRI) was performed 0 to 3 hours, and 1, 2, 7, and 14 days after an impact to the primary forelimb somatosensory cortex. Behavioral assessments were performed before injury induction and before MRI scans on days 2, 7, and 14. Nissl staining was performed on day 14 to corroborate the lesion volume detected from MRI. Contrary to our hypothesis, we found that NBO treatment increased lesion volume in a rat model of moderate TBI and had no positive effect on behavioral measures. Our results do not promote the acute use of NBO in patients with moderate TBI.

Neuroprotective effects of mildronate in a rat model of traumatic brain injury

Injury ◽  
2019 ◽  
Vol 50 (10) ◽  
pp. 1586-1592 ◽  
Author(s):  
Dilan Demir ◽  
Pınar Kuru Bektaşoğlu ◽  
Türkan Koyuncuoğlu ◽  
Cansu Kandemir ◽  
Dilek Akakın ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Rat Model ◽  
Neuroprotective Effects

scholarly journals Hypoxia preconditioning protects neuronal cells against traumatic brain injury through stimulation of glucose transport mediated by HIF-1α/GLUTs signaling pathway in rat

2020 ◽  
Author(s):  
Xiaogang Wu ◽  
Chunlin Wang ◽  
Jinbiao Wang ◽  
Meijie Zhu ◽  
Yinsheng Yao ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Cerebral Cortex ◽  
Brain Injury ◽  
Glucose Transport ◽  
Hypoxia Tolerance ◽  
Tunel Staining ◽  
Transport Activity ◽  
Neuroprotective Effects ◽  
Hypoxia Preconditioning ◽  
Cerebral Cortex Tissue

AbstractHypoxia preconditioning (HPC), a well-established preconditioning model, has been shown to protect the brain against severe hypoxia or ischemia caused by traumatic brain injury (TBI), but the mechanism has not been well elucidated. Anaerobic glycolysis is the major way for neurons to produce energy under cerebral ischemia and hypoxia after TBI, and it requires large amounts of glucose. We hypothesized that glucose transport, as a rate-limiting step of glucose metabolism, may play key roles in the neuroprotective effects of HPC on cerebral cortex tissue against TBI. The aim of this study was to investigate the effect of HPC on glucose transport activity of rat cerebral cortex tissue after TBI through examining the gene expression of two major glucose transporters (GLUT1 and GLUT3) and their upstream target gene hypoxia-inducible factor-1α (HIF-1α). Sprague-Dawley rats were treated with HPC (50.47 kPa, 3 h/d, 3d). Twenty-four hours after the last treatment, the rats were injured using the Feeney free falling model. Cortex tissues of injured rats were removed at 1 h, 4 h, 8 h, 12 h, 1 day, 3 days, 7 d, and 14 days post-injury for histological analysis. Compared with TBI alone, HPC before TBI resulted in the expression of HIF-1α, GLUT1, and GLUT3 to increase at 1 h; they were markedly increased at 4 h, 8 h, 12 h, 1 day, and 3 days and decreased thereafter (p < 0.05). HPC before TBI could improve neuronal survival in rats by examining NeuN staining and observing reduced apoptosis by examining TUNEL staining. The result showed that HPC before TBI could increase the expression of GLUT1 and GLUT3. And through double immunofluorescence staining for GLUT3 and NeuN, the results strongly suggest that HPC improved glucose transport activity of neurons in rats with TBI. In summary, our results further support that HPC can improve hypoxia tolerance and attenuate neuronal loss of cerebral cortex in rats after TBI. The mechanism is mainly related to the increase of glucose transport activity through inducing GLUT1 and GLUT3 expression through upregulating HIF-1α expression.

scholarly journals C1q/CTRP1 exerts neuroprotective effects in TBI rats by regulating inflammation and autophagy

2020 ◽  
Author(s):  
Ming Pei ◽  
Chaoqun Wang ◽  
Zhengdong Li ◽  
Jianhua Zhang ◽  
Ping Huang ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Underlying Mechanism ◽  
Inflammatory Factors ◽  
Vehicle Group ◽  
Secondary Brain Injury ◽  
Neuroprotective Effects ◽  
Cerebral Ischemia Reperfusion Injury

AbstractObjectiveC1q/CTRP1 is a newly discovered adiponectin protein, which is highly expressed in adipose and heart tissues. Recent studies have revealed that C1q/CTRP1 can regulate metabolism and inhibit inflammation. CTRP1 is also expressed in brain tissues and vascular cells of human and rat, and research on cerebral hemorrhage and cerebral ischemia-reperfusion injury demonstrates that the CTRP family can attenuate secondary brain injury and exert neuroprotective effects. Thus, this study was designed to explore the role of CTRP1 in traumatic brain injury (TBI) and the underlying mechanism.Main methodsRats were assigned into rCTRP1 group, vehicle group, and sham group. Modified Feeney’s method was used to establish a closed traumatic brain injury model. Morris water maze was used for directional navigation, reverse searching and space exploration tests in rats. In addition, Golgi-Cox staining was utilized to visualize neurons, dendrites and dendritic spines. ELISA was conducted to detect the levels of inflammatory factors (IL-6 and TNF-α). Finally, Western blot was adopted to detect the relative expression of p-mTOR and autophagy-related proteins (Beclin-1 and LC3-II).ResultsCTRP1 improved the behavioral and histopathological outcomes, inhibited the inflammatory response, activated mTOR and decreased autophagy-associated protein synthesis in TBI rats.ConclusionCTRP1 exerts neuroprotective effects in TBI rats by regulating inflammation and autophagy and has potential therapeutic properties after TBI.

Sign in / Sign up

Export Citation Format

Share Document