scholarly journals Neuroprotective effects of oleocanthal, a compound in virgin olive oil, in a rat model of traumatic brain injury

Author(s):  
Mesut Mete ◽  
Isil Aydemir ◽  
Ulkun Unlu Unsal ◽  
Fatih Collu ◽  
Gokhan Vatandas ◽  
...  
2022 ◽  
Vol 20 (2) ◽  
pp. 293-299
Author(s):  
Xueliang Gao ◽  
Zhao Wang ◽  
Peilei Jia ◽  
Yapeng Zhao ◽  
Kai Wang ◽  
...  

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.


2018 ◽  
Vol 112 ◽  
pp. e278-e287 ◽  
Author(s):  
Sher-Wei Lim ◽  
Eric Nyam TT ◽  
Cho-Ya Hu ◽  
Chung-Ching Chio ◽  
Che-Chuan Wang ◽  
...  

2020 ◽  
pp. 1-13
Author(s):  
Milka Perović ◽  
Milena Jović ◽  
Smilja Todorović ◽  
Aleksandra Mladenović Đorđević ◽  
Desanka Milanović ◽  
...  

2016 ◽  
Vol 86 ◽  
pp. 243-249 ◽  
Author(s):  
İsmail Gülşen ◽  
Hakan Ak ◽  
Neşe Çölçimen ◽  
Hamit H. Alp ◽  
Mehmet E. Akyol ◽  
...  

Injury ◽  
2019 ◽  
Vol 50 (10) ◽  
pp. 1586-1592 ◽  
Author(s):  
Dilan Demir ◽  
Pınar Kuru Bektaşoğlu ◽  
Türkan Koyuncuoğlu ◽  
Cansu Kandemir ◽  
Dilek Akakın ◽  
...  

2020 ◽  
Vol 12 (1) ◽  
pp. 001-008
Author(s):  
Ting Liu ◽  
Xing-Zhi Liao ◽  
Mai-Tao Zhou

Abstract Background Brain edema is one of the major causes of fatality and disability associated with injury and neurosurgical procedures. The goal of this study was to evaluate the effect of ulinastatin (UTI), a protease inhibitor, on astrocytes in a rat model of traumatic brain injury (TBI). Methodology A rat model of TBI was established. Animals were randomly divided into 2 groups – one group was treated with normal saline and the second group was treated with UTI (50,000 U/kg). The brain water content and permeability of the blood–brain barrier were assessed in the two groups along with a sham group (no TBI). Expression of the glial fibrillary acidic protein, endthelin-1 (ET-1), vascular endothelial growth factor (VEGF), and matrix metalloproteinase 9 (MMP-9) were measured by immunohistochemistry and western blot. Effect of UTI on ERK and PI3K/AKT signaling pathways was measured by western blot. Results UTI significantly decreased the brain water content and extravasation of the Evans blue dye. This attenuation was associated with decreased activation of the astrocytes and ET-1. UTI treatment decreased ERK and Akt activation and inhibited the expression of pro-inflammatory VEGF and MMP-9. Conclusion UTI can alleviate brain edema resulting from TBI by inhibiting astrocyte activation and ET-1 production.


2021 ◽  
Vol 341 ◽  
pp. 113698
Author(s):  
William T. O'Brien ◽  
Louise Pham ◽  
Rhys D. Brady ◽  
Jesse Bain ◽  
Glenn R. Yamakawa ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document