PMID- 28198521
OWN - NLM
STAT- MEDLINE
DCOM- 20180507
LR  - 20220310
IS  - 1898-018X (Electronic)
IS  - 1898-018X (Linking)
VI  - 24
IP  - 4
DP  - 2017
TI  - Sevoflurane ameliorates doxorubicin-induced myocardial injury by affecting the 
      phosphorylation states of proteins in PI3K/Akt/mTOR signaling pathway.
PG  - 409-418
LID - 10.5603/CJ.a2017.0018 [doi]
AB  - BACKGROUND: The effect of sevoflurane on the doxorubicin-induced myocardial 
      injury was explored by investigating the phosphorylation states of proteins in 
      phosphatidylinositol 3-kinase (PI3K)/Akt/mam-malian target of rapamycin (mTOR) 
      signaling pathway. METHODS: Myocardial injury rat models were induced by 
      doxorubicin and evenly assigned into five groups according to different 
      treatment: Doxorubicin group (DG, 200-muL saline solution), sevoflurane group 
      (SevG, inhaled with 2.4% sevoflurane for 2 h), LY294002 group (LYG, Akt 
      inhibitor, 0.3 mg/kg in 200-muL Dimethyl Sulfoxide [DMSO]), solvent DMSO control 
      group (SG) and autophagy inhibitor 3-methyladenine (3-MA) group (MG, 30 mg/kg in 
      200-muL DMSO). The healthy rats were assigned to a contro1 group (CG, 200-muL 
      saline solution). Myocardial apoptosis was detected by terminal deoxynucleotidyl 
      transferase dUTP nick end labeling (TUNEL) assay. The concentration of cardiac 
      troponin I (cTnI) was detected by ELISA. The levels of total Akt (t-Akt), 
      phosphorylated Akt (p-Akt), mammalian target of rapamycin (mTOR), 
      phosphorylated-mTOR (p-mTOR) and autophagy marker LC3-II was detected by Western 
      Blot. The experiments were also repeated at the cell level. RESULTS: Terminal 
      deoxynucleotidyl transferase dUTP nick end labeling analysis showed that the 
      ap-optosis rates were high in DG and SG, reached the highest level in LYG, 
      reduced in SevG and MG, and reached the lowest level in CG. The levels of p-Akt 
      p-mTOR were low in groups DG and SG, reached the lowest level in LYG, increased 
      in SevG and MG, and reached the highest level in CG. In contrast, LC3-II 
      expression, apoptosis index and serum cTnI concentration were high in DG and SG, 
      reached the highest level in LYG, reduced in SevG and MG, and reached the lowest 
      level in CG (p < 0.05). Cell experiment showed similar results as with animal 
      experiments. CONCLUSIONS: Sevoflurane ameliorates myocardial injury by affecting 
      the phosphorylation states of the proteins in PI3K/Akt/mTOR signaling pathway and 
      reducing the injury biomarker. (Cardiol J 2017; 24, 4: 409-418).
FAU - Wu, Yini
AU  - Wu Y
FAU - Wang, Jianping
AU  - Wang J
FAU - Yu, Xiaoyan
AU  - Yu X
FAU - Li, Dongli
AU  - Li D
FAU - Han, Xin
AU  - Han X
FAU - Fan, Lihua
AU  - Fan L
AD  - Department of General surgery,Wenzhou Medical College, the fifth Affiliated 
      Hospital. fanlihua19@126.com.
LA  - eng
PT  - Journal Article
DEP - 20170215
PL  - Poland
TA  - Cardiol J
JT  - Cardiology journal
JID - 101392712
RN  - 0 (Methyl Ethers)
RN  - 0 (Protective Agents)
RN  - 0 (Troponin I)
RN  - 38LVP0K73A (Sevoflurane)
RN  - 80168379AG (Doxorubicin)
RN  - EC 1.1.1.27 (L-Lactate Dehydrogenase)
RN  - EC 2.7.1.1 (mTOR protein, rat)
RN  - EC 2.7.1.137 (Phosphatidylinositol 3-Kinase)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 2.7.3.2 (Creatine Kinase, MB Form)
SB  - IM
MH  - Animals
MH  - Apoptosis/drug effects
MH  - Cardiotoxicity
MH  - Cell Line
MH  - Creatine Kinase, MB Form/metabolism
MH  - Cytoprotection
MH  - Disease Models, Animal
MH  - *Doxorubicin
MH  - Heart Diseases/chemically induced/enzymology/pathology/*prevention & control
MH  - L-Lactate Dehydrogenase/metabolism
MH  - Methyl Ethers/*pharmacology
MH  - Myocardium/*enzymology/pathology
MH  - Phosphatidylinositol 3-Kinase/*metabolism
MH  - Phosphorylation
MH  - Protective Agents/*pharmacology
MH  - Proto-Oncogene Proteins c-akt/*metabolism
MH  - Rats, Sprague-Dawley
MH  - Sevoflurane
MH  - Signal Transduction/drug effects
MH  - TOR Serine-Threonine Kinases/*metabolism
MH  - Troponin I/metabolism
OTO - NOTNLM
OT  - cardiac injury
OT  - doxorubicin
OT  - phosphatidylinositol 3-kinase
OT  - phosphorylated rapamycin
OT  - protein-serine-threonine kinases
EDAT- 2017/02/16 06:00
MHDA- 2018/05/08 06:00
CRDT- 2017/02/16 06:00
PHST- 2016/09/12 00:00 [received]
PHST- 2016/11/23 00:00 [accepted]
PHST- 2017/02/09 00:00 [revised]
PHST- 2017/02/16 06:00 [pubmed]
PHST- 2018/05/08 06:00 [medline]
PHST- 2017/02/16 06:00 [entrez]
AID - VM/OJS/J/48774 [pii]
AID - 10.5603/CJ.a2017.0018 [doi]
PST - ppublish
SO  - Cardiol J. 2017;24(4):409-418. doi: 10.5603/CJ.a2017.0018. Epub 2017 Feb 15.