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 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.

Premarin stimulates estrogen receptor-α to protect against traumatic brain injury in male rats*

2009 ◽  
Vol 37 (12) ◽  
pp. 3097-3106 ◽  
Author(s):  
Sheng-Hsien Chen ◽  
Chia-Yu Chang ◽  
Hsiu-Kang Chang ◽  
Wei-Chun Chen ◽  
Mao-Tsun Lin ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Estrogen Receptor ◽  
Brain Injury ◽  
Estrogen Receptor Α ◽  
Male Rats

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

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

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

The effect of female sexual hormones on the intestinal and serum cytokine response after traumatic brain injury: different roles for estrogen receptor subtypes

2013 ◽  
Vol 91 (9) ◽  
pp. 700-707 ◽  
Author(s):  
Mohammad Khaksari ◽  
Zakieh Keshavarzi ◽  
Ahmad Gholamhoseinian ◽  
Bahram Bibak
Keyword(s):  
Traumatic Brain Injury ◽  
Estrogen Receptor ◽  
Brain Injury ◽  
Treated Group ◽  
Estrogen Receptor Α ◽  
Female Rats ◽  
Receptor Subtypes ◽  
Sexual Hormones ◽  
Tnf Α ◽  
Vehicle Treated Group

The purpose of this study was to evaluate the effect of female sexual hormones on intestinal and serum cytokines following traumatic brain injury (TBI). Adult female rats were ovariectomized and distributed among the following 9 groups: (i) sham trauma, (ii) TBI (Marmarou’s method), (iii) vehicle (dimethylsulfoxide) treated, (iv) estrogen (E2) treated, (v) progesterone (P) treated, (vi) treated with E2+P, (vii) propylpyrazole triol (PPT) treated, (viii) diarylpropionitrile (DPN) treated, and (ix) control. PPT and DPN are estrogen receptor αand β agonists, respectively. Serum and intestinal levels of interleukin (IL)-1β were increased by TBI (P < 0.001). The level of intestinal IL-1β was increased in the group treated with E2 (P < 0.001). There was a reduction in serum IL-1β (P < 0.01) and an increase in intestinal IL-1β level (P < 0.001) in the PPT-treated group compared with the vehicle-treated group. TBI reduced serum IL-6 (P < 0.01) and increased intestinal IL-6 (P < 0.001). Serum IL-6 was increased in the group treated with E2 (P < 0.001), P (P < 0.001), E2+P (P < 0.01), and DPN (P < 0.001) after TBI; however, intestinal IL-6 was higher in the E2-treated group compared with the vehicle-treated group (P < 0.01). Intestinal tumor necrosis factor α (TNF-α) was increased by TBI (P < 0.001). Progesterone decreased serum TNF-α (P < 0.01). Intestinal TNF-α in the E2 (P < 0.01), E2+P (P < 0.001), and PPT (P < 0.001) treatment groups was less than in the vehicle-treated group. In conclusion, estrogen influences the intestinal levels of proinflammatory cytokines, in particular TNF-α, mediated through estrogen receptor α.

scholarly journals Ulinastatin alleviates traumatic brain injury by reducing endothelin-1

2020 ◽  
Vol 12 (1) ◽  
pp. 001-008
Author(s):  
Ting Liu ◽  
Xing-Zhi Liao ◽  
Mai-Tao Zhou
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Western Blot ◽  
Water Content ◽  
Brain Edema ◽  
Rat Model ◽  
Neurosurgical Procedures ◽  
Brain Water Content ◽  
The Brain ◽  
Brain Water

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.

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