PMID- 32329866
OWN - NLM
STAT- MEDLINE
DCOM- 20210329
LR  - 20210329
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 24
IP  - 7
DP  - 2020 Apr
TI  - Research on mechanism of sevoflurane in alleviating cerebral ischemia-reperfusion 
      injury in rats through JNK signaling pathway.
PG  - 3907-3914
LID - 20857 [pii]
LID - 10.26355/eurrev_202004_20857 [doi]
AB  - OBJECTIVE: To explore the specific mechanism of sevoflurane in alleviating 
      cerebral ischemia-reperfusion injury (CIRI) in rats through the c-Jun N-terminal 
      kinase (JNK) signaling pathway. MATERIALS AND METHODS: A total of 60 male 
      specific pathogen-free Sprague-Dawley rats were randomly divided into sham group 
      (n=20), model group (n=20), and sevoflurane group (n=20). In the sevoflurane 
      group, sevoflurane (2.5%) was inhaled for 60 min at 24 h before the blockage of 
      cerebral blood supply. The CIRI model was established using the suture method in 
      the model group and sevoflurane group, while the right common carotid artery and 
      external carotid artery were separated and ligated only, without suture 
      placement, in the sham group. At 24 h after reperfusion, the neurological deficit 
      score in each group was calculated, the water content in brain tissues in each 
      group was detected based on dry-wet weight ratio, the infarction volume of brain 
      tissues in each group was detected via 2,3,5-triphenyltetrazolium chloride (TTC) 
      staining, and the apoptosis rate of brain cells in each group was detected using 
      terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) 
      assay. Moreover, the protein levels of JNK, p-JNK, B-cell lymphoma-2 (Bcl-2), and 
      the Bcl-2 associated X protein (Bax) in brain tissues were determined using 
      Western blotting, and the gene expressions of Bax and Bcl-2 in brain tissues were 
      determined through fluorescence quantitative Polymerase Chain Reaction (qPCR). 
      RESULTS: It was found that the water content in brain tissues and the cerebral 
      infarction volume were significantly increased in the model group compared with 
      those in the sham group (p<0.01, p<0.01), while they were notably decreased in 
      the sevoflurane group compared with those in the model group (p<0.05, p<0.01). 
      The neurological deficit score was significantly higher in the model group than 
      that in the sham group (p<0.01), while it was remarkably lower in the sevoflurane 
      group than that in the model group (p<0.01). According to the results of the 
      TUNEL assay, the model group had an evidently higher apoptosis rate of brain 
      cells than the sham group (p<0.01), while the sevoflurane group had a lower 
      apoptosis rate of brain cells than the model group (p<0.05). Besides, the results 
      of Western blotting revealed that the model group exhibited remarkably increased 
      protein levels of JNK, p-JNK, and Bax (p<0.05, p<0.01, p<0.01) and a remarkably 
      decreased protein level of Bcl-2 (p<0.01) compared with the sham group. 
      Sevoflurane group had decreased protein levels of JNK, p-JNK, and Bax (p<0.05, 
      p<0.01, p<0.01) and an increased protein level of Bcl-2 (p<0.05) in comparison 
      with the model group. In addition, the gene expression of Bcl-2 significantly 
      declined (p<0.01), and that of Bax remarkably rose (p<0.01) in the model group 
      compared with those in the sham group, while the contrary is the case in the 
      sevoflurane group compared with those in the model group (p<0.05, p<0.01). 
      CONCLUSIONS: Sevoflurane can regulate the protein and gene expressions of Bax and 
      Bcl-2 and reduce apoptosis in CIRI by regulating the JNK signaling pathway, 
      thereby exerting a protective effect on brain tissues and improving the symptoms 
      of neurological deficit.
FAU - Hu, C-Y
AU  - Hu CY
AD  - Department of Anesthesiology, Shanxi Medical University, Taiyuan, China. 
      guoyongqingselina@163.com.
FAU - Guo, Y-Q
AU  - Guo YQ
FAU - Hao, Y-H
AU  - Hao YH
FAU - Zheng, L-N
AU  - Zheng LN
FAU - Qi, Y-H
AU  - Qi YH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Italy
TA  - Eur Rev Med Pharmacol Sci
JT  - European review for medical and pharmacological sciences
JID - 9717360
RN  - 38LVP0K73A (Sevoflurane)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Animals
MH  - Apoptosis/drug effects
MH  - JNK Mitogen-Activated Protein Kinases/*metabolism
MH  - Male
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reperfusion Injury/*drug therapy/metabolism/pathology
MH  - Sevoflurane/*pharmacology
MH  - Signal Transduction/*drug effects
EDAT- 2020/04/25 06:00
MHDA- 2021/03/30 06:00
CRDT- 2020/04/25 06:00
PHST- 2020/04/25 06:00 [entrez]
PHST- 2020/04/25 06:00 [pubmed]
PHST- 2021/03/30 06:00 [medline]
AID - 20857 [pii]
AID - 10.26355/eurrev_202004_20857 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2020 Apr;24(7):3907-3914. doi: 
      10.26355/eurrev_202004_20857.