Biphalin, a dimeric opioid peptide, reduces neonatal hypoxia-ischemia brain injury in mice by the activation of PI3K/Akt signaling pathway

Author(s):  
Jin-Jia Zhang ◽  
Yuan Li ◽  
Su Chen ◽  
Xiao-Fei Yang ◽  
Jia-Wei Min
Oncotarget ◽  
2017 ◽  
Vol 8 (58) ◽  
pp. 97977-97989 ◽  
Author(s):  
Guangming Tang ◽  
Huiyun Yang ◽  
Jing Chen ◽  
Mengrao Shi ◽  
Lingqing Ge ◽  
...  

ASN NEURO ◽  
2021 ◽  
Vol 13 ◽  
pp. 175909142110384
Author(s):  
Han Xiao ◽  
Jianyang Liu ◽  
Jialin He ◽  
Ziwei Lan ◽  
Mingyang Deng ◽  
...  

Estrogen is neuroprotective in brain injury models, and steroid receptor cofactor 3 (SRC3) mediates estrogen signaling. We aimed to investigate whether and how SRC3 is involved in the neuroprotective effects of 17ß-estradiol (E2) in a mouse model of intracerebral hemorrhage (ICH). Ovariectomized female mice were treated with E2 after autologous blood injection-induced ICH. Brain damage was assessed by neurological deficit score, brain water content, and oxidative stress levels. Blood–brain barrier (BBB) integrity was evaluated by Evan's blue extravasation and claudin-5, ZO-1, and occludin levels. SRC3 expression and PI3K/Akt signaling pathway were examined in ICH mice treated with E2. The effect of SRC3 on E2-mediated neuroprotection was determined by examining neurological outcomes in SRC3-deficient mice undergone ICH and E2 treatment. We found that E2 alleviated ICH-induced brain edema and neurological deficits, protected BBB integrity, and suppressed oxidative stress. E2 enhanced SRC3 expression and PI3K-/Akt signaling pathway. SRC3 deficiency abolished the protective effects of E2 on ICH-induced neurological deficits, brain edema, and BBB integrity. Our results suggest that E2 suppresses ICH-induced brain injury and SRC3 plays a critical role in E2-mediated neuroprotection.


2014 ◽  
Vol 1587 ◽  
pp. 15-22 ◽  
Author(s):  
Xiao-ke Hao ◽  
Wei Wu ◽  
Chun-xi Wang ◽  
Guang-bin Xie ◽  
Tao Li ◽  
...  

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