Publication: Albiflorin relieves cerebral ischemia-reperfusion
injury by activating Nrf2/HO-1 pathway
Authors
Zhu, Fei ; Xiong, Jianzhong ; Yi, Fei ; Luo, Ermin ; Huang, Chun ; Li, Runying
item.page.secondaryauthor
item.page.director
Publisher
Universidad de Murcia, Departamento de Biologia Celular e Histiologia
publication.page.editor
publication.page.department
DOI
https://doi.org/10.14670/HH-18-518
item.page.type
info:eu-repo/semantics/article
Description
Abstract
Our work aims to investigate the functions of
a natural compound, Albiflorin (AF) in cerebral
ischemia-reperfusion (IR) injury. The cerebral IR models
were established by OGD/R in PC12 cells and
MCAO/IR in rats. The cells in a glucose-free medium
were placed in an anaerobic chamber containing 95% N2 and 5% CO2 for 3h at 37°C, returned to a normal
medium, and incubated for 24h to accomplish OGD/R.
Focal cerebral ischemia was conducted by thread
occlusion of the right middle cerebral artery for 2h
followed by 24h reperfusion in rats. CCK-8 assay
indicated that AF had no toxicity to PC12 cells. Flow
cytometry, Western blot, or TUNEL showed that AF
treatment reduced apoptosis of cells or rat brain tissues.
qRT-PCR and ELISA showed that AF decreased IL-1β,
IL-6, and TNF-α levels in vitro and in vivo. Elevated
levels of MDA, SOD, and ROS induced by IR injury
were mitigated by AF in vitro and in vivo. HE and TTC
staining revealed that AF ameliorated pathological injury
in MCAO/IR rats. Western blot showed that Nrf2,
NQO1, and HO-1 expression was activated by AF, and
ML385 treatment suppressed the inhibition effects of AF
in cerebral IR injury models. Overall, AF alleviates
cerebral IR injury via regulating the Nrf2/HO-1 pathway.
publication.page.subject
Citation
Histology and Histopathology Vol. 38, nº2 (2023)
item.page.embargo
Ir a Estadísticas
Este ítem está sujeto a una licencia Creative Commons. http://creativecommons.org/licenses/by-nc-nd/4.0/