Propofol protects human cardiac AC16 cells from CoCl2-induced hypoxic injury.
10.11817/j.issn.1672-7347.2019.03.012
- Author:
Liu HAN
1
,
2
;
Xiaodan ZHANG
3
;
Yanning QIAN
4
Author Information
1. Department of Anesthesiology, First Affiliated Hospital, Nanjing Medical University, Nanjing 210029
2. Department of Anesthesiology, Nanjing Hospital Affiliated to Nanjing Medical University (Nanjing First Hospital), Nanjing 210006, China.
3. Department of Anesthesiology, Nanjing Hospital Affiliated to Nanjing Medical University (Nanjing First Hospital), Nanjing 210006, China.
4. Department of Anesthesiology, First Affiliated Hospital, Nanjing Medical University, Nanjing 210029, China.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
Cell Hypoxia;
Cell Line;
Cell Survival;
Cobalt;
pharmacology;
Humans;
Hypoxia;
JNK Mitogen-Activated Protein Kinases;
Propofol;
Reactive Oxygen Species
- From:
Journal of Central South University(Medical Sciences)
2019;44(3):307-314
- CountryChina
- Language:Chinese
-
Abstract:
To explore the effect of propofol on human cardiac AC16 cells under CoCl2-induced hypoxic injury and the possible mechanisms.
Methods: Human AC16 cardiomyocytes were treated with cobalt chloride (CoCl2) to mimic hypoxic condition in cultured cardiomyocytes. The AC16 cells were divided into 3 groups: a control group, a CoCl2 hypoxia group (CoCl2 group), and a propofol+CoCl2 group (propofol+ CoCl2 group). The cell viability was assessed by cell counting kit-8 (CCK-8). Cell apoptosis ratio (AR) and the mitochondrial membrane potential (Δψm) were detected by flow cytometry. The reactive oxygen species (ROS) production in AC16 cells were determined with the ROS-sensitive fluorescent probe. Meanwhile, total intracellular levels of malondialdehyde (MDA) and superoxide dismutase (SOD) in AC16 cells were detected with commercially available kits. Western blot was used to evaluate the activation of c-Jun N-terminal kinase (JNK) and p38 signaling pathways.
Results: 1) Compared with the control group, AC16 cell viability was decreased significantly in the CoCl2 group following the treatment with 500 μmol/L CoCl2 (P<0.01); 2) Compared with the control group, AR value in AC16 cells was increased significantly in the CoCl2 group, while Δψm was decreased significantly (all P<0.01). Compared with the CoCl2 group, AR value in AC16 cells was decreased significantly in the propofol+CoCl2 group, while Δψm was increased significantly (both P<0.05); 3) Compared with the control group, the levels of ROS and MDA were increased significantly, and the level of SOD was significantly decreased in the CoCl2 group (all P<0.01). Compared with the CoCl2 group, the ROS and MDA levels in the propofol+CoCl2 group were increased significantly and the SOD levels were decreased significantly (all P<0.05); 4) Compared with the control group, the phosphorylation levels of JNK and p38 were increased significantly (both P<0.05) in the CoCl2 group. Compared with the CoCl2 group, the phosphorylation levels of JNK and p38 were decreased significantly in the propofol+CoCl2 group (both P<0.05).
Conclusion: The pretreatment with propofol may protect human cardiac AC16 cells from the chemical hypoxia-induced injury through regulation of JNK and p38 signaling pathways.
