Oleanolic acid reduces oxidative stress and neuronal apoptosis after experimental subarachnoid hemorrhage by regulating Nrf2/ HO ‐1 pathway

2021 ◽  
Author(s):  
Yuwei Han ◽  
Chenchen Wang ◽  
Xiaoming Li ◽  
Guobiao Liang
Keyword(s):  
Oxidative Stress ◽  
Subarachnoid Hemorrhage ◽  
Oleanolic Acid ◽  
Neuronal Apoptosis ◽  
Experimental Subarachnoid Hemorrhage

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

scholarly journals AVE 0991 attenuates oxidative stress and neuronal apoptosis via Mas/PKA/CREB/UCP-2 pathway after subarachnoid hemorrhage in rats

Redox Biology ◽  
2019 ◽  
Vol 20 ◽  
pp. 75-86 ◽  
Author(s):  
Jun Mo ◽  
Budbazar Enkhjargal ◽  
Zachary D. Travis ◽  
Keren Zhou ◽  
Pei Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Subarachnoid Hemorrhage ◽  
Neuronal Apoptosis

The Role of Oxidative Stress in Microvascular Disturbances after Experimental Subarachnoid Hemorrhage

2019 ◽  
Vol 10 (6) ◽  
pp. 684-694 ◽  
Author(s):  
Toshio Fumoto ◽  
Masato Naraoka ◽  
Takeshi Katagai ◽  
Yuchen Li ◽  
Norihito Shimamura ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Subarachnoid Hemorrhage ◽  
Experimental Subarachnoid Hemorrhage

scholarly journals Sodium/Hydrogen Exchanger 1 Participates in Early Brain Injury after Subarachnoid Hemorrhage both in vivo and in vitro via Promoting Neuronal Apoptosis

2019 ◽  
Vol 28 (8) ◽  
pp. 985-1001 ◽  
Author(s):  
Huangcheng Song ◽  
Shuai Yuan ◽  
Zhuwei Zhang ◽  
Juyi Zhang ◽  
Peng Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Brain Edema ◽  
Neuronal Apoptosis ◽  
Early Brain Injury ◽  
Sodium Hydrogen ◽  
Sodium Hydrogen Exchanger

Sodium/hydrogen exchanger 1 (NHE1) plays an essential role in maintaining intracellular pH (pHi) homeostasis in the central nervous system (CNS) under physiological conditions, and it is also associated with neuronal death and intracellular Na+ and Ca2+ overload induced by cerebral ischemia. However, its roles and underlying mechanisms in early brain injury (EBI) induced by subarachnoid hemorrhage (SAH) have not been fully explored. In this research, a SAH model in adult male rat was established through injecting autologous arterial blood into prechiasmatic cistern. Meanwhile, primary cultured cortical neurons of rat treated with 5 μM oxygen hemoglobin (OxyHb) for 24 h were applied to mimic SAH in vitro. We find that the protein levels of NHE1 are significantly increased in brain tissues of rats after SAH. Downregulation of NHE1 by HOE642 (a specific chemical inhibitor of NHE1) and genetic-knockdown can effectively alleviate behavioral and cognitive dysfunction, brain edema, blood-brain barrier (BBB) injury, inflammatory reactions, oxidative stress, neurondegeneration, and neuronal apoptosis, all of which are involved in EBI following SAH. However, upregulation of NHE1 by genetic-overexpression can produce opposite effects. Additionally, inhibiting NHE1 significantly attenuates OxyHb-induced neuronal apoptosis in vitro and reduces interaction of NHE1 and CHP1 both in vivo and in vitro. Collectively, we can conclude that NHE1 participates in EBI induced by SAH through mediating inflammation, oxidative stress, behavioral and cognitive dysfunction, BBB injury, brain edema, and promoting neuronal degeneration and apoptosis.

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