PMID- 32014567
OWN - NLM
STAT- MEDLINE
DCOM- 20210817
LR  - 20230416
IS  - 1873-2747 (Electronic)
IS  - 0361-9230 (Linking)
VI  - 157
DP  - 2020 Apr
TI  - Sodium aescinate provides neuroprotection in experimental traumatic brain injury 
      via the Nrf2-ARE pathway.
PG  - 26-36
LID - S0361-9230(19)30198-4 [pii]
LID - 10.1016/j.brainresbull.2020.01.019 [doi]
AB  - Sodium aescinate (SA), a natural plant extract, has been proven to provide 
      neuroprotection in neurological diseases. However, its role and the underlying 
      pathophysiological mechanisms in traumatic brain injury (TBI) are still not well 
      understood. The present study was aimed to investigate the protective effects of 
      SA in both in vivo and in vitro TBI models. Mice or neurons were randomly divided 
      into control, TBI, TBI + vehicle and TBI + SA groups. Neurologic severity score 
      (NSS) was used to evaluate the neurological impairment. Brain water content and 
      lesion volume were used to assess the brain injury degree. Malondialdehyde (MDA) 
      and glutathione peroxidase (GPx) levels were used to estimate oxidative stress. 
      Western blot was used to determine the protein levels. Nissl and terminal 
      deoxynucleotidyl transferase-mediated dUTP nick 3'-end labeling (TUNEL) staining 
      were used to measure cell death and apoptosis. Our results revealed that 
      treatment of SA could improve neurological function, decrease cerebral edema and 
      attenuate brain lesion after TBI. Furthermore, administration of SA suppressed 
      TBI-induced oxidative stress, neuron cell death and apoptosis. In addition, SA 
      activated the nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant 
      response element (ARE) pathway after TBI. However, SA failed to provide 
      neuroprotection following TBI in Nrf2(-/-) mice. Taken together, our results 
      provided the first evidence that SA treatment played a key role in 
      neuroprotection after TBI through the Nrf2-ARE pathway.
CI  - Copyright (c) 2020 Elsevier Inc. All rights reserved.
FAU - Zhang, Li
AU  - Zhang L
AD  - Department of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing 
      University, Nanjing, Jiangsu Province, PR China.
FAU - Fei, Maoxing
AU  - Fei M
AD  - Department of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing 
      University, Nanjing, Jiangsu Province, PR China.
FAU - Wang, Handong
AU  - Wang H
AD  - Department of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing 
      University, Nanjing, Jiangsu Province, PR China. Electronic address: 
      njhdwang@hotmail.com.
FAU - Zhu, Yihao
AU  - Zhu Y
AD  - Department of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing 
      University, Nanjing, Jiangsu Province, PR China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20200131
PL  - United States
TA  - Brain Res Bull
JT  - Brain research bulletin
JID - 7605818
RN  - 0 (NF-E2-Related Factor 2)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Saponins)
RN  - 0 (Triterpenes)
RN  - 0 (sodium aescinate)
SB  - IM
EIN - Brain Res Bull. 2023 Jun 15;198:1-2. PMID: 37062115
MH  - Animals
MH  - Antioxidant Response Elements/*drug effects
MH  - Brain/drug effects/metabolism
MH  - Brain Injuries/*drug therapy/pathology
MH  - Brain Injuries, Traumatic/*blood/*drug therapy/pathology
MH  - Disease Models, Animal
MH  - Male
MH  - Mice, Inbred ICR
MH  - NF-E2-Related Factor 2/drug effects/metabolism
MH  - Neurons/drug effects
MH  - Neuroprotection/drug effects
MH  - Neuroprotective Agents/pharmacology
MH  - Oxidative Stress/drug effects
MH  - Saponins/*metabolism
MH  - Triterpenes/*metabolism
OTO - NOTNLM
OT  - Apoptosis
OT  - Neuroprotection
OT  - Nrf2-ARE pathway
OT  - Oxidative stress
OT  - Sodium aescinate
OT  - Traumatic brain injury
COIS- Declaration of Competing Interest The authors declare no potential conflicts of 
      interest.
EDAT- 2020/02/06 06:00
MHDA- 2021/08/18 06:00
CRDT- 2020/02/05 06:00
PHST- 2019/03/12 00:00 [received]
PHST- 2019/12/17 00:00 [revised]
PHST- 2020/01/24 00:00 [accepted]
PHST- 2020/02/06 06:00 [pubmed]
PHST- 2021/08/18 06:00 [medline]
PHST- 2020/02/05 06:00 [entrez]
AID - S0361-9230(19)30198-4 [pii]
AID - 10.1016/j.brainresbull.2020.01.019 [doi]
PST - ppublish
SO  - Brain Res Bull. 2020 Apr;157:26-36. doi: 10.1016/j.brainresbull.2020.01.019. Epub 
      2020 Jan 31.