PMID- 34055311
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230920
IS  - 2045-452X (Print)
IS  - 2045-4538 (Electronic)
IS  - 2045-452X (Linking)
VI  - 8
IP  - 6
DP  - 2019 Nov 1
TI  - Astilbin attenuates cerebral ischemia/reperfusion injury by inhibiting the 
      TLR4/MyD88/NF-kappaB pathway.
PG  - 1002-1008
LID - 10.1039/c9tx00222g [doi]
AB  - Ischemic stroke is the second most common cause of death worldwide and cerebral 
      ischemia/reperfusion (I/R) injury also leads to serious tissue damage. Astilbin, 
      a natural bioactive flavonoid compound, has been reported to have protective 
      effects on neurological diseases. This study aims to investigate the effects of 
      astilbin on cerebral I/R injury and determine the mechanisms involved. The 
      results demonstrated that, in cerebral I/R rats, astilbin could attenuate I/R 
      injury in the hippocampal region, decreasing the activity of lactate 
      dehydrogenase (LDH) and malondialdehyde (MDA) in the rat brain. Astilbin also 
      inhibited the I/R-induced upregulation of pro-inflammatory mediators (TNFalpha, 
      IL-1beta, IL-6). Similarly, in hypoxia/reperfusion (H/R) treated human neuroblastoma 
      cells, astilbin could increase the cell viability of SH-SY5Y, decrease the 
      activity of LDH and MDA, and inhibit the H/R-induced upregulation of 
      pro-inflammatory mediators. For the mechanism study, western blot results 
      indicated that astilbin could inhibit the expression of Toll-like receptor 4 
      (TLR4), myeloid differential protein 88 (MYD88) and phosphorylated NF-kappaB p65 in 
      H/R treated SH-SY5Y cells. The research indicated that astilbin ameliorated 
      cerebral I/R injury partly via the TLR4/MyD88/NF-kappaB pathway. Astilbin may have 
      potential therapeutic effects on cerebral ischemia.
CI  - This journal is (c) The Royal Society of Chemistry 2019.
FAU - Li, Jing
AU  - Li J
AUID- ORCID: 0000-0001-5199-1703
AD  - Changchun University of Chinese Medicine , Changchun City , Jilin Province 130000 
      , China . Email: JingLisdf@163.com ; Tel: +86-0431-81953783.
FAU - Gu, Zhaowei
AU  - Gu Z
AD  - Changchun University of Chinese Medicine , Changchun City , Jilin Province 130000 
      , China . Email: JingLisdf@163.com ; Tel: +86-0431-81953783.
FAU - Liu, Yue
AU  - Liu Y
AD  - Changchun University of Chinese Medicine , Changchun City , Jilin Province 130000 
      , China . Email: JingLisdf@163.com ; Tel: +86-0431-81953783.
FAU - Wang, Yu
AU  - Wang Y
AD  - Changchun University of Chinese Medicine , Changchun City , Jilin Province 130000 
      , China . Email: JingLisdf@163.com ; Tel: +86-0431-81953783.
FAU - Zhao, Min
AU  - Zhao M
AD  - Changchun University of Chinese Medicine , Changchun City , Jilin Province 130000 
      , China . Email: JingLisdf@163.com ; Tel: +86-0431-81953783.
LA  - eng
PT  - Journal Article
DEP - 20191118
PL  - England
TA  - Toxicol Res (Camb)
JT  - Toxicology research
JID - 101587950
ECI - Toxicol Res (Camb). 2021 Apr 16;10(3):662. PMID: 34136124
PMC - PMC8142934
EDAT- 2019/11/18 00:00
MHDA- 2019/11/18 00:01
PMCR- 2020/11/18
CRDT- 2021/05/31 06:13
PHST- 2019/08/20 00:00 [received]
PHST- 2019/10/18 00:00 [accepted]
PHST- 2021/05/31 06:13 [entrez]
PHST- 2019/11/18 00:00 [pubmed]
PHST- 2019/11/18 00:01 [medline]
PHST- 2020/11/18 00:00 [pmc-release]
AID - c9tx00222g [pii]
AID - 10.1039/c9tx00222g [doi]
PST - epublish
SO  - Toxicol Res (Camb). 2019 Nov 18;8(6):1002-1008. doi: 10.1039/c9tx00222g. 
      eCollection 2019 Nov 1.