Journal article
Propofol Ameliorates H9c2 Cells Apoptosis Induced by Oxygen Glucose Deprivation and Reperfusion Injury via Inhibiting High Levels of Mitochondrial Fusion and Fission
Frontiers in pharmacology, Vol.10, pp.61-61
02/12/2019
DOI: 10.3389/fphar.2019.00061
PMCID: PMC6379462
PMID: 30809145
Abstract
Background:
The cardioprotective effect of propofol on ischemia-reperfusion injury (I/R injury) is partly due to suppressing apoptosis. Mitochondrial dynamics are also involved in apoptosis. Mitochondrial fusion and fission lead to mitochondrial morphological changes. However, whether suppressing apoptosis effect of propofol against ischemia-reperfusion injury in the heart is via regulating mitochondrial morphology remains unclear.
Methods:
H9c2 cells underwent oxygen glucose deprivation (OGD) followed by reperfusion to simulate cardiomyocytes ischemia/reperfusion injury. Cell viability, apoptosis ratio and intracellular reactive oxygen species (ROS) were assessed, respectively. Mitochondrial membrane dynamin family proteins, extracellular signal regulated kinase 1 and 2 (ERK1/2), phosphorylated extracellular signal regulated kinase 1 and 2 (p-ERK1/2) and proteins related to intrinsic apoptosis pathways were detected by western blotting. The mitochondrial morphology and the distribution of dynamin-related protein 1 (Drp1) were observed by using laser confocal microscopy.
Results:
Propofol enhanced the survival of H9c2 cells, decreased ROS levels and inhibited apoptosis during oxygen glucose deprivation/reperfusion (OGD/R) injury. Mitochondrial fission in H9c2 cells was inhibited by propofol during OGD injury. Propofol alleviated high levels of mitochondrial fusion and fission during OGD/R in H9c2 cells, by regulating mitochondrial membrane remodeling dynamin family proteins. Propofol inhibited Drp1 colocalization with mitochondria in H9c2 cells during OGD/R injury. Moreover, Drp1 phosphorylation was inhibited by propofol through decreasing ERK activation during OGD/R injury. We found that propofol ameliorated H9c2 cells apoptosis during OGD/R via inhibiting mitochondrial cytochrome c release and caspase-9, caspase-6, caspase-7 and caspase-3 activation.
Conclusion:
Propofol suppresses H9c2 cells apoptosis during OGD/R injury via inhibiting intrinsic apoptosis pathway, which may be partly due to reducing high levels of mitochondrial fusion and fission induced by OGD/R injury.
Details
- Title: Subtitle
- Propofol Ameliorates H9c2 Cells Apoptosis Induced by Oxygen Glucose Deprivation and Reperfusion Injury via Inhibiting High Levels of Mitochondrial Fusion and Fission
- Creators
- Lidong Zhao - Shanghai First People's HospitalJinqiang Zhuang - Shanghai Jiao Tong UniversityYihui Wang - Shanghai First People's HospitalDandan Zhou - Shanghai First People's HospitalDandan Zhao - Shanghai First People's HospitalShun Zhu - Shanghai Jiao Tong UniversityJinjun Pu - Shanghai University of Traditional Chinese MedicineHongyu Zhang - University of BergenMing Yin - Shanghai Jiao Tong UniversityWenjuan Zhao - Shanghai Jiao Tong UniversityZejian Wang - Shanghai Jiao Tong UniversityJiang Hong - , , , , , , , ,
- Resource Type
- Journal article
- Publication Details
- Frontiers in pharmacology, Vol.10, pp.61-61
- Publisher
- Frontiers Media S.A
- DOI
- 10.3389/fphar.2019.00061
- PMID
- 30809145
- PMCID
- PMC6379462
- ISSN
- 1663-9812
- eISSN
- 1663-9812
- Grant note
- 81570293; 81471232 / National Natural Science Foundation of China
- Language
- English
- Date published
- 02/12/2019
- Academic Unit
- Internal Medicine
- Record Identifier
- 9984696754302771
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