PMID- 32432772
OWN - NLM
STAT- MEDLINE
DCOM- 20210331
LR  - 20210331
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 24
IP  - 9
DP  - 2020 May
TI  - Sevoflurane inhibits neuronal apoptosis and expressions of HIF-1 and HSP70 in 
      brain tissues of rats with cerebral ischemia/reperfusion injury.
PG  - 5082-5090
LID - 21201 [pii]
LID - 10.26355/eurrev_202005_21201 [doi]
AB  - OBJECTIVE: To observe the influences of sevoflurane on neuronal apoptosis and 
      expressions of hypoxia-inducible factor 1 (HIF-1), and heat-shock protein 70 
      (HSP70) in brain tissues of rats with cerebral ischemia/reperfusion (I/R) injury. 
      MATERIALS AND METHODS: A total of 60 Sprague-Dawley rats were selected and 
      divided into sham-operation group (Sham group, n=20), cerebral I/R model group 
      (Model group, n=20), and 3% sevoflurane treatment group (Sevoflurane group, 
      n=20). The rats in each group received neurological scoring, and the blood and 
      brain tissues were collected to detect the concentrations of serum K+, Na+ and 
      glucose (Glu). Enzyme-linked immunosorbent assay (ELISA) was adopted to measure 
      the levels of inflammatory factors [tumor necrosis factor-beta (TNF-beta) and 
      interleukin-6 (IL-6)] and oxidative stress [catalase (CAT), malondialdehyde (MDA) 
      and superoxide dismutase (SOD)]. Terminal deoxynucleotidyl transferase-mediated 
      dUTP nick end labeling (TUNEL) assay was performed to determine the nerve cell 
      apoptosis in the brain tissues. The gene and protein expressions of Caspase-3, 
      HIF-1, and HSP70 in the brain tissues were measured via quantitative Reverse 
      Transcription-Polymerase Chain Reaction (qRT-PCR) and Western blotting. RESULTS: 
      In Sevoflurane group, the content of serum Glu and Na+ was decreased markedly, 
      that of K+ was increased notably, and the levels of TNF-beta, IL-1 and IL-6 were 
      lowered remarkably compared with those in Model group (p<0.05). Moreover, the 
      neurological score was reduced evidently (p<0.05). Model group had significantly 
      strengthened the activity of MDA and CAT and decreased SOD content, while 
      Sevoflurane group exhibited the opposite results. TUNEL staining showed that 
      there were distinctly more apoptotic cells that were dominated by glial cells in 
      Model group and fewer apoptotic cells in Sevoflurane group. It was indicated in 
      gene assay that the messenger ribonucleic acid (mRNA) expression levels of HIF-1, 
      HSP70, and Caspase-3 in Model group were remarkably higher than those in Sham 
      group and Sevoflurane group (p<0.05). According to the results of Western 
      blotting, the protein expressions of HIF-1 and HSP70 in Sevoflurane group were 
      markedly lower than those in Model group. CONCLUSIONS: Sevoflurane can reduce the 
      content of inflammatory factors, inhibit apoptosis, and reduce the expressions of 
      HIF-1 and HSP70 in the case of cerebral I/R injury, thus exerting protective 
      effects on rats with cerebral I/R injury.
FAU - Yu, F
AU  - Yu F
AD  - Department of Anesthesiology, The First Hospital of China Medical University, 
      Shenyang, China. cds1225@sina.com.
FAU - Tong, L-J
AU  - Tong LJ
FAU - Cai, D-S
AU  - Cai DS
LA  - eng
PT  - Journal Article
PL  - Italy
TA  - Eur Rev Med Pharmacol Sci
JT  - European review for medical and pharmacological sciences
JID - 9717360
RN  - 0 (HSP70 Heat-Shock Proteins)
RN  - 0 (Hypoxia-Inducible Factor 1)
RN  - 38LVP0K73A (Sevoflurane)
SB  - IM
MH  - Animals
MH  - Apoptosis/drug effects
MH  - Brain/drug effects/metabolism/pathology
MH  - Disease Models, Animal
MH  - HSP70 Heat-Shock Proteins/*antagonists & inhibitors/genetics/metabolism
MH  - Hypoxia-Inducible Factor 1/*antagonists & inhibitors/genetics/metabolism
MH  - Infarction, Middle Cerebral Artery/*drug therapy/metabolism/pathology
MH  - Male
MH  - Neurons/*drug effects/metabolism/pathology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reperfusion Injury/*drug therapy/metabolism/pathology
MH  - Sevoflurane/administration & dosage/*pharmacology
EDAT- 2020/05/21 06:00
MHDA- 2021/04/01 06:00
CRDT- 2020/05/21 06:00
PHST- 2020/05/21 06:00 [entrez]
PHST- 2020/05/21 06:00 [pubmed]
PHST- 2021/04/01 06:00 [medline]
AID - 21201 [pii]
AID - 10.26355/eurrev_202005_21201 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2020 May;24(9):5082-5090. doi: 
      10.26355/eurrev_202005_21201.