scholarly journals 3,4-Dihydroxyphenylethanol alleviates early brain injury by modulating oxidative stress and Akt and nuclear factor-κB pathways in a rat model of subarachnoid hemorrhage

2016 ◽  
Vol 11 (5) ◽  
pp. 1999-2004 ◽  
Author(s):  
PENG FU ◽  
QUAN HU
Keyword(s):  
Oxidative Stress ◽  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Rat Model ◽  
Early Brain Injury ◽  
Nuclear Factor Κb ◽  
Nuclear Factor

Treatment of early brain injury after subarachnoid hemorrhage in the rat model by inhibiting p53-induced ferroptosis

2021 ◽  
pp. 136134
Author(s):  
Hong Kuang ◽  
Tianhong Wang ◽  
Lei Liu ◽  
Chunhai Tang ◽  
Tao Li ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Rat Model ◽  
Early Brain Injury

Apigenin attenuates oxidative stress and neuronal apoptosis in early brain injury following subarachnoid hemorrhage

2017 ◽  
Vol 40 ◽  
pp. 157-162 ◽  
Author(s):  
Yuwei Han ◽  
Tingting Zhang ◽  
Jingyuan Su ◽  
Yuan Zhao ◽  
Chenchen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Neuronal Apoptosis ◽  
Early Brain Injury

Tetramethylpyrazine Protects Against Early Brain Injury and Inhibits the PERK/Akt Pathway in a Rat Model of Subarachnoid Hemorrhage

2018 ◽  
Vol 43 (8) ◽  
pp. 1650-1659 ◽  
Author(s):  
Zhengkai Shao ◽  
Pei Wu ◽  
Xuefeng Wang ◽  
Meishan Jin ◽  
Shuang Liu ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Rat Model ◽  
Early Brain Injury ◽  
Akt Pathway

PARP inhibition attenuates early brain injury through NF-κB/MMP-9 pathway in a rat model of subarachnoid hemorrhage

2016 ◽  
Vol 1644 ◽  
pp. 32-38 ◽  
Author(s):  
Ting Chen ◽  
Wei Wang ◽  
Jian-Ru Li ◽  
Hang-Zhe Xu ◽  
Yu-Cong Peng ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Rat Model ◽  
Early Brain Injury ◽  
Parp Inhibition

Amelioration of oxidative stress and protection against early brain injury by astaxanthin after experimental subarachnoid hemorrhage

2014 ◽  
Vol 121 (1) ◽  
pp. 42-54 ◽  
Author(s):  
Xiang-Sheng Zhang ◽  
Xin Zhang ◽  
Meng-Liang Zhou ◽  
Xiao-Ming Zhou ◽  
Ning Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Oral Administration ◽  
Brain Edema ◽  
Blood Brain Barrier ◽  
Early Brain Injury ◽  
Antioxidant Property ◽  
Neural Cell ◽  
Intracerebroventricular Injection

Object Aneurysmal subarachnoid hemorrhage (SAH) causes devastating rates of mortality and morbidity. Accumulating studies indicate that early brain injury (EBI) greatly contributes to poor outcomes after SAH and that oxidative stress plays an important role in the development of EBI following SAH. Astaxanthin (ATX), one of the most common carotenoids, has a powerful antioxidative property. However, the potential role of ATX in protecting against EBI after SAH remains obscure. The goal of this study was to assess whether ATX can attenuate SAH-induced brain edema, blood-brain barrier permeability, neural cell death, and neurological deficits, and to elucidate whether the mechanisms of ATX against EBI are related to its powerful antioxidant property. Methods Two experimental SAH models were established, including a prechiasmatic cistern SAH model in rats and a one-hemorrhage SAH model in rabbits. Both intracerebroventricular injection and oral administration of ATX were evaluated in this experiment. Posttreatment assessments included neurological scores, body weight loss, brain edema, Evans blue extravasation, Western blot analysis, histopathological study, and biochemical estimation. Results It was observed that an ATX intracerebroventricular injection 30 minutes post-SAH could significantly attenuate EBI (including brain edema, blood-brain barrier disruption, neural cell apoptosis, and neurological dysfunction) after SAH in rats. Meanwhile, delayed treatment with ATX 3 hours post-SAH by oral administration was also neuroprotective in both rats and rabbits. In addition, the authors found that ATX treatment could prevent oxidative damage and upregulate the endogenous antioxidant levels in the rat cerebral cortex following SAH. Conclusions These results suggest that ATX administration could alleviate EBI after SAH, potentially through its powerful antioxidant property. The authors conclude that ATX might be a promising therapeutic agent for EBI following SAH.

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