PMID- 31275755
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220409
IS  - 2167-8359 (Print)
IS  - 2167-8359 (Electronic)
IS  - 2167-8359 (Linking)
VI  - 7
DP  - 2019
TI  - Sevoflurane postconditioning alleviates hypoxia-reoxygenation injury of 
      cardiomyocytes by promoting mitochondrial autophagy through the HIF-1/BNIP3 
      signaling pathway.
PG  - e7165
LID - 10.7717/peerj.7165 [doi]
LID - e7165
AB  - BACKGROUND: Sevoflurane postconditioning (SpostC) can alleviate 
      hypoxia-reoxygenation injury of cardiomyocytes; however, the specific mechanism 
      remains unclear. This study aimed to investigate whether SpostC promotes 
      mitochondrial autophagy through the hypoxia-inducible factor-1 
      (HIF-1)/BCL2/adenovirus E1B 19-kDa-interacting protein 3 (BNIP3) signaling 
      pathway to attenuate hypoxia-reoxygenation injury in cardiomyocytes. METHODS: The 
      H9C2 cardiomyocyte hypoxia/reoxygenation model was established and treated with 
      2.4% sevoflurane at the beginning of reoxygenation. Cell damage was determined by 
      measuring cell viability, lactate dehydrogenase activity, and apoptosis. 
      Mitochondrial ultrastructural and autophagosomes were observed by transmission 
      electron microscope. Western blotting was used to examine the expression of 
      HIF-1, BNIP3, and Beclin-1 proteins. The effects of BNIP3 on promoting autophagy 
      were determined using interfering RNA technology to silence BNIP3. RESULTS: 
      Hypoxia-reoxygenation injury led to accumulation of autophagosomes in 
      cardiomyocytes, and cell viability was significantly reduced, which seriously 
      damaged cells. Sevoflurane postconditioning could upregulate HIF-1alpha and BNIP3 
      protein expression, promote autophagosome clearance, and reduce cell damage. 
      However, these protective effects were inhibited by 2-methoxyestradiol or 
      sinBNIP3. CONCLUSION: Sevoflurane postconditioning can alleviate 
      hypoxia-reoxygenation injury in cardiomyocytes, and this effect may be achieved 
      by promoting mitochondrial autophagy through the HIF-1/BNIP3 signaling pathway.
FAU - Yang, Long
AU  - Yang L
AD  - Department of Anesthesiology, The First Affiliated Hospital of Xinjiang Medical 
      University, Urumqi, Xinjiang, China.
FAU - Wu, Jianjiang
AU  - Wu J
AD  - Department of Anesthesiology, The First Affiliated Hospital of Xinjiang Medical 
      University, Urumqi, Xinjiang, China.
FAU - Xie, Peng
AU  - Xie P
AD  - Department of Anesthesiology, Zunyi Medical College, Guizhou Key Laboratory of 
      Anesthesia and Organ Protection, Zunyi, Guizhou, China.
FAU - Yu, Jin
AU  - Yu J
AD  - Chongqing Health Center for Women and Children, Department of Anesthesiology, 
      Chongqing, Chongqing, China.
FAU - Li, Xin
AU  - Li X
AD  - Department of Anesthesiology, The First Affiliated Hospital of Xinjiang Medical 
      University, Urumqi, Xinjiang, China.
FAU - Wang, Jiang
AU  - Wang J
AD  - Department of Anesthesiology, The First Affiliated Hospital of Xinjiang Medical 
      University, Urumqi, Xinjiang, China.
FAU - Zheng, Hong
AU  - Zheng H
AD  - Department of Anesthesiology, The First Affiliated Hospital of Xinjiang Medical 
      University, Urumqi, Xinjiang, China.
LA  - eng
PT  - Journal Article
DEP - 20190624
PL  - United States
TA  - PeerJ
JT  - PeerJ
JID - 101603425
PMC - PMC6596409
OTO - NOTNLM
OT  - Autophagy
OT  - Hypoxia-reoxygenation injury
OT  - Myocardial protection
OT  - Sevoflurane postconditioning
COIS- The authors declare that they have no competing interests.
EDAT- 2019/07/06 06:00
MHDA- 2019/07/06 06:01
PMCR- 2019/06/24
CRDT- 2019/07/06 06:00
PHST- 2019/01/17 00:00 [received]
PHST- 2019/05/22 00:00 [accepted]
PHST- 2019/07/06 06:00 [entrez]
PHST- 2019/07/06 06:00 [pubmed]
PHST- 2019/07/06 06:01 [medline]
PHST- 2019/06/24 00:00 [pmc-release]
AID - 7165 [pii]
AID - 10.7717/peerj.7165 [doi]
PST - epublish
SO  - PeerJ. 2019 Jun 24;7:e7165. doi: 10.7717/peerj.7165. eCollection 2019.