Propofol postconditioning ameliorates hypoxia/reoxygenation induced H9c2 cell apoptosis and autophagy <italic style="font-style: italic">via</italic> upregulating forkhead transcription factors under hyperglycemia

Rong-Hui Han; He-Meng Huang; Hong Han; Hao Chen; Fei Zeng; Xiang Xie; Dan-Yong Liu; Yin Cai; Liang-Qing Zhang; Xin Liu; Zheng-Yuan Xia; Jing Tang

doi:10.1186/s40779-021-00353-0

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Propofol postconditioning ameliorates hypoxia/reoxygenation induced H9c2 cell apoptosis and autophagy via upregulating forkhead transcription factors under hyperglycemia

RESEARCH | Updated：2023-02-28

- Propofol postconditioning ameliorates hypoxia/reoxygenation induced H9c2 cell apoptosis and autophagy via upregulating forkhead transcription factors under hyperglycemia
- Propofol postconditioning ameliorates hypoxia/reoxygenation induced H9c2 cell apoptosis and autophagy via upregulating forkhead transcription factors under hyperglycemia
- 解放军医学杂志（英文版） 2022年9卷第3期页码：286-302
- Affiliations：
  
  1.Department of Anesthesiology, Affiliated Hospital of Guangdong Medical University, 57 South Renming Avenue Xiashan District, Zhanjiang 524000, Guangdong, China
  2.Department of Emergency, Affiliated Hospital of Guangdong Medical University, Zhanjiang 524000, Guangdong, China
  3.Department of Anesthesiology, the Eighth Affiliated Hospital, Sun Yat-Sen University, Guangzhou 518000, China
  4.Department of Anesthesiology, Guangzhou First People’s Hospital, the Second Affiliated Hospital of South China University of Technology, Guangzhou 510000, China
  5.Department of Anesthesiology, the Second Affiliated Hospital and Yuying Children’s Hospital, Wenzhou Medical University, Wenzhou 325000, Zhejiang, China
  6.Department of Health Technology and Informatics, the Hong Kong Polytechnic University, Hung Hom 999077, Hong Kong SAR, China
  7.State Key Laboratory of Pharmaceutical Biotechnology, Department of Medicine, the University of Hong Kong, Pok Fu Lam 999077, Hong Kong SAR, China
- Author bio：
  
  * zyxia@hku.hk;
  tanglitangjing@126.com
- Funds：
  
  the National Natural Science Foundation of China grant(NSFC81970247)
- DOI：10.1186/s40779-021-00353-0
  中图分类号：
- 纸质出版：2022-06
- Accepted：
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Propofol postconditioning ameliorates hypoxia/reoxygenation induced H9c2 cell apoptosis and autophagy via upregulating forkhead transcription factors under hyperglycemia[J]. 解放军医学杂志（英文版）, 2022,9(3):286-302.

Han et al.: Propofol postconditioning ameliorates hypoxia/reoxygenation induced H9c2 cell apoptosis and autophagy via upregulating forkhead transcription factors under hyperglycemia. Mil Med Res, 2021, 8: 58.
Propofol postconditioning ameliorates hypoxia/reoxygenation induced H9c2 cell apoptosis and autophagy via upregulating forkhead transcription factors under hyperglycemia[J]. 解放军医学杂志（英文版）, 2022,9(3):286-302. DOI： 10.1186/s40779-021-00353-0.

Han et al.: Propofol postconditioning ameliorates hypoxia/reoxygenation induced H9c2 cell apoptosis and autophagy via upregulating forkhead transcription factors under hyperglycemia. Mil Med Res, 2021, 8: 58. DOI： 10.1186/s40779-021-00353-0.

摘要

Abstract

Background:

Administration of propofol

an intravenous anesthetic with antioxidant property

immediately at the onset of post-ischemic reperfusion (propofol postconditioning

P-PostC) has been shown to confer cardioprotection against ischemia–reperfusion (I/R) injury

while the underlying mechanism remains incompletely understood. The forkhead box O (FoxO) transcription factors are reported to play critical roles in activating cardiomyocyte survival signaling throughout the process of cellular injuries induced by oxidative stress and are also involved in hypoxic postconditioning mediated neuroprotection

however

the role of FoxO in postconditioning mediated protection in the heart and in particular in high glucose condition is unknown.

Methods:

Rat heart-derived H9c2 cells were exposed to high glucose (HG) for 48 h

then subjected to hypoxia/reoxygenation (H/R

composed of 8 h of hypoxia followed by 12 h of reoxygenation) in the absence or presence of postconditioning with various concentrations of propofol (P-PostC) at the onset of reoxygenation. After having identified the optical concentration of propofol

H9c2 cells were subjected to H/R and P-PostC in the absence or presence of FoxO1 or FoxO3a gene silencing to explore their roles in P-PostC mediated protection against apoptotic and autophagic cell deaths under hyperglycemia.

Results:

The results showed that HG with or without H/R decreased cell viability

increased lactate dehydrogenase (LDH) leakage and the production of reactive oxygen species (ROS) in H9c2 cells

all of which were significantly reversed by propofol (P-PostC)

especially at the concentration of 25 μmol/L (P25) (

0.05

. HG; HG

. HG+HR; HG+HR+P12.5 or HG+HR+P25 or HG+HR+P50

. HG+HR). Moreover

we found that propofol (P25) decreased H9c2 cells apoptosis and autophagy that were concomitant with increased FoxO1 and FoxO3a expression (

0.05

HG+HR+P25

. HG+HR). The protective effects of propofol (P25) against H/R injury were reversed by silencing FoxO1 or FoxO3a (

0.05

HG+HR+P25

. HG+HR+P25+siRNA-1 or HG+HR+P25+siRNA-5).

Conclusions:

It is concluded that propofol postconditioning attenuated H9c2 cardiac cells apoptosis and autophagy induced by H/R injury through upregulating FoxO1 and FoxO3a under hyperglycemia.

关键词

Keywords

references

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Propofol postconditioning ameliorates hypoxia/reoxygenation induced H9c2 cell apoptosis and autophagy via upregulating forkhead transcription factors under hyperglycemia

Propofol postconditioning ameliorates hypoxia/reoxygenation induced H9c2 cell apoptosis and autophagy via upregulating forkhead transcription factors under hyperglycemia

DOI：10.1186/s40779-021-00353-0

摘要

Abstract

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Keywords

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