Neuroprotective effect of apigenin against hypoxic-ischemic brain injury in neonatal rats via activation of the PI3K/Akt/Nrf2 signaling pathway

2021 ◽  
Author(s):  
Changchang Fu ◽  
Yihui Zheng ◽  
Kun Lin ◽  
Hongzeng Wang ◽  
Tingting Chen ◽  
...  
Keyword(s):  
Cerebral Palsy ◽  
Brain Injury ◽  
Signaling Pathway ◽  
Neuroprotective Effect ◽  
Ischemic Brain Injury ◽  
Neonatal Rats ◽  
Ischemic Brain ◽  
Nrf2 Signaling Pathway ◽  
Hypoxic Ischemic Brain Injury

Neonatal hypoxic-ischemic (HI) brain injury can lead to mortality and severe long-term disabilities including cerebral palsy and brain injury.

Neuroprotective effect of human placental extract on hypoxic–ischemic brain injury in neonatal rats

2013 ◽  
Vol 35 (1) ◽  
pp. 68-74 ◽  
Author(s):  
Jee Yoon Park ◽  
Jung Hye Byeon ◽  
Sung-Won Park ◽  
So-Hee Eun ◽  
Kyu Young Chae ◽  
...  
Keyword(s):  
Brain Injury ◽  
Neuroprotective Effect ◽  
Ischemic Brain Injury ◽  
Neonatal Rats ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury ◽  
Placental Extract

scholarly journals Neuroprotective Effect of Cycloheximide on Hypoxic-Ischemic Brain Injury in Neonatal Rats

2006 ◽  
Vol 21 (2) ◽  
pp. 337 ◽  
Author(s):  
Won Soon Park ◽  
Dong Kyung Sung ◽  
Saem Kang ◽  
Soo Hyun Koo ◽  
Yu Jin Kim ◽  
...  
Keyword(s):  
Brain Injury ◽  
Neuroprotective Effect ◽  
Ischemic Brain Injury ◽  
Neonatal Rats ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury

Neuroprotective effect of nipradilol, an NO donor, on hypoxic–ischemic brain injury of neonatal rats

2007 ◽  
Vol 83 (8) ◽  
pp. 535-540 ◽  
Author(s):  
Hiroko Kakizawa ◽  
Fumiko Matsui ◽  
Yoshihito Tokita ◽  
Kanako Hirano ◽  
Michiru Ida ◽  
...  
Keyword(s):  
Brain Injury ◽  
Neuroprotective Effect ◽  
Ischemic Brain Injury ◽  
Neonatal Rats ◽  
No Donor ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury

scholarly journals Sevoflurane Post-Conditioning Alleviated Hypoxic-Ischemic Brain Injury in Neonatal Rats by Inhibiting Endoplasmic Reticulum Stress-Mediated Autophagy via IRE1 Signalings

2021 ◽  
Author(s):  
Jiayuan Niu ◽  
Ziyi Wu ◽  
Hang Xue ◽  
Yahan Zhang ◽  
Qiushi Gao ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Brain Injury ◽  
Er Stress ◽  
Signaling Pathway ◽  
Ischemic Brain Injury ◽  
Neonatal Rats ◽  
Artery Ligation ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury ◽  
The Relationship

Abstract Post-conditioning with sevoflurane, a volatile anesthetic, has been proved to be neuroprotective against hypoxic-ischemic brain injury (HIBI). Our previous research showed that autophagy is over-activated in a rat model of neonatal HIBI, and inhibition of autophagy confers neuroprotection. There is increasing recognition that autophagy can be triggered by activating endoplasmic reticulum (ER) stress. This study aimed to explore: i) the relationship between ER stress and autophagy in the setting of neonatal HIBI; and ii) the possible roles of ER stress-mediated autophagy and IRE1 signalings in the neuroprotection of sevoflurane post-conditioning against neonatal HIBI. Seven-day-old rats underwent left common artery ligation followed by 2 h hypoxia (8% O2 / 92% N2). The relationship between ER stress and autophagy was examined by ER stress inducer (tunicamycin), ER stress inhibitor (4-PBA), or autophagy inhibitor (3-MA). Rats in the sevoflurane post-conditioning groups were treated with 2.4% sevoflurane for 30 min after HIBI induction. The roles of ER stress-mediated autophagy and the IRE1/JNK/beclin1 signaling pathway in the neuroprotection afforded by sevoflurane were examined by ER stress inducer (tunicamycin) and the IRE1 inhibitor (STF-083010). HIBI over‑activated ER stress and autophagy in neonatal rats. HIBI-induced autophagy was significantly aggravated by tunicamycin but blocked by 4-PBA; however, HIBI-induced ER stress was not affected by 3-MA. Sevoflurane post-conditioning significantly alleviated ER stress, autophagy, cell apoptosis, and cognitive impairments, which were remarkably abolished by tunicamycin. Also, tunicamycin blocked sevoflurane-induced downregulation of IRE1/JNK/beclin1 signaling pathway. Whereas, IRE1 inhibitor could reverse the effects of tunicamycin. ER stress contributes to autophagy induced by HIBI. Furthermore, sevoflurane post-conditioning significantly protects against HIBI in neonatal rats by inhibiting ER stress-mediated autophagy via IRE1/JNK/beclin1 signaling pathway.

Neuroprotective effect of levetiracetam on hypoxic ischemic brain injury in neonatal rats

2014 ◽  
Vol 30 (6) ◽  
pp. 1001-1009 ◽  
Author(s):  
Mustafa Komur ◽  
Cetin Okuyaz ◽  
Yalcin Celik ◽  
Bora Resitoglu ◽  
Ayse Polat ◽  
...  
Keyword(s):  
Brain Injury ◽  
Neuroprotective Effect ◽  
Ischemic Brain Injury ◽  
Neonatal Rats ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury
Sign in / Sign up

Export Citation Format

Share Document