PMID- 29710456
OWN - NLM
STAT- MEDLINE
DCOM- 20180917
LR  - 20211204
IS  - 1950-6007 (Electronic)
IS  - 0753-3322 (Linking)
VI  - 99
DP  - 2018 Mar
TI  - Vitexin reverses the autophagy dysfunction to attenuate MCAO-induced cerebral 
      ischemic stroke via mTOR/Ulk1 pathway.
PG  - 583-590
LID - S0753-3322(17)36302-3 [pii]
LID - 10.1016/j.biopha.2018.01.067 [doi]
AB  - Stroke, as a kind of acute cerebrovascular diseases, has greatly influenced the 
      patients' quality of life and left a huge public health burden. Vitexin is a 
      flavone C-glycoside (apigenin-8-C-?-D-glucopyranoside) present in several 
      medicinal and other plants. This study aims to explore the role of vitexin in 
      middle cerebral artery occlusion (MCAO)-induced cerebral ischemic stroke. The 
      results showed that the MCAO-induced brain infarction was obviously decreased by 
      vitexin. And the abnormal protein levels of Caspase-3, Bcl-2-associated X protein 
      (Bax), antigen identified by monoclonal antibody (Ki-67) and B cell lymphoma 2 
      (Bcl-2) in MCAO model rats were reversed by vitexin. Further research indicated 
      that vitexin alleviated MCAO-induced oxidative injury by reducing the levels of 
      lactate dehydrogenase (LDH), malondialdehyde (MDA) and nitric Oxide (NO). In 
      addition, vitexin attenuated the secretion of pro-inflammatory cytokine 
      (interleukin (IL)-6 and tumor necrosis factor alpha (TNF-?)) and increased 
      anti-inflammatory cytokine (IL-10) production to ameliorate MCAO-induced 
      inflammation. What's more, vitexin repressed the MCAO-induced autophagy through 
      mechanistic target of rapamycin (mTOR)/Ulk1 pathway. Specifically, the 
      MCAO-induced decreased expression of mTOR, peroxisome proliferator-activated 
      receptor ? (PPAR?) and p62 were inhibited by vitexin. At the same time, 
      MCAO-induced increased expression of Ulk1, Beclin1 and rate of LC3?/LC3? also 
      were repressed by vitexin. But the inhibition of vitexin on the MCAO-induced 
      oxidative injury, apoptosis and inflammation were reversed by rapamycin. These 
      results implied that vitexin suppressed the autophagy dysfunction to attenuate 
      MCAO-induced cerebral ischemic stroke via mTOR/Ulk1 pathway.
CI  - Copyright (c) 2018. Published by Elsevier Masson SAS.
FAU - Jiang, Jin
AU  - Jiang J
AD  - Department of Neurology, Central Hospital of Hanzhong City, Shaanxi Province, 
      723000, PR China.
FAU - Dai, Jingcun
AU  - Dai J
AD  - ICU of Liaocheng Third People's Hospital, Liaocheng, Shandong Province, 252000, 
      PR China.
FAU - Cui, Hong
AU  - Cui H
AD  - Electroencephalogram Room, The First Hospital of Yulin, Shaanxi Province, 719000, 
      PR China. Electronic address: hongcui123@outlook.com.
LA  - eng
PT  - Journal Article
DEP - 20180220
PL  - France
TA  - Biomed Pharmacother
JT  - Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
JID - 8213295
RN  - 7V515PI7F6 (Apigenin)
RN  - 9VP70K75OK (vitexin)
RN  - EC 2.7.1.1 (mTOR protein, rat)
RN  - EC 2.7.11.1 (Autophagy-Related Protein-1 Homolog)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 2.7.11.1 (ULK1 protein, rat)
RN  - W36ZG6FT64 (Sirolimus)
SB  - IM
MH  - Animals
MH  - Apigenin/*pharmacology
MH  - Apoptosis/drug effects
MH  - Autophagy/*drug effects
MH  - Autophagy-Related Protein-1 Homolog/metabolism
MH  - Brain Ischemia/*drug therapy/pathology
MH  - Disease Models, Animal
MH  - Infarction, Middle Cerebral Artery/complications
MH  - Inflammation/drug therapy/pathology
MH  - Male
MH  - Oxidative Stress/drug effects
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Sirolimus/pharmacology
MH  - Stroke/*drug therapy/pathology
MH  - TOR Serine-Threonine Kinases/metabolism
OTO - NOTNLM
OT  - Apoptosis
OT  - Autophagy
OT  - Cerebral ischemic stroke
OT  - Inflammation
OT  - Oxidative injury
OT  - Vitexin
OT  - mTOR/Ulk1 pathway
EDAT- 2018/05/02 06:00
MHDA- 2018/09/18 06:00
CRDT- 2018/05/02 06:00
PHST- 2017/11/22 00:00 [received]
PHST- 2018/01/08 00:00 [revised]
PHST- 2018/01/11 00:00 [accepted]
PHST- 2018/05/02 06:00 [entrez]
PHST- 2018/05/02 06:00 [pubmed]
PHST- 2018/09/18 06:00 [medline]
AID - S0753-3322(17)36302-3 [pii]
AID - 10.1016/j.biopha.2018.01.067 [doi]
PST - ppublish
SO  - Biomed Pharmacother. 2018 Mar;99:583-590. doi: 10.1016/j.biopha.2018.01.067. Epub 
      2018 Feb 20.