MoS2 nanozyme attenuated inflammation-related endothelial cell injury by regulating mitochondrial dynamics and mitophagy
10.16438/j.0513-4870.2024-0416
- VernacularTitle:MoS2纳米酶通过调控线粒体动力及自噬减轻炎性内皮细胞损伤
- Author:
Dong-mei PAN
1
;
Sun-kui KE
2
;
Qian-hao YIN
3
;
Pei-yan YANG
4
;
Chao LI
1
;
She-fang YE
3
Author Information
1. The HaiChuang Hospital of Xiamen Medical College, Xiamen 361000, China
2. Zhongshan Hospital of Xiamen University, Xiamen 361004, China
3. The Higher Educational Key Laboratory for Biomedical Engineering of Fujian Province, Department of Biomaterials, Research Center of Biomedical Engineering of Xiamen, Xiamen University, Xiamen 361005, China
4. The First Affiliated Hospital of Xiamen University, Xiamen 361004, China
- Publication Type:Research Article
- Keywords:
MoS2 nanozyme;
vascular endothelium;
oxidative stress;
mitochondrial dynamics;
mitophagy
- From:
Acta Pharmaceutica Sinica
2024;59(10):2791-2799
- CountryChina
- Language:Chinese
-
Abstract:
To explore the protective mechanisms of a novel molybdenum disulfide (MoS2) nanozyme in alleviating inflammation-related endothelial cell injury by regulating mitochondrial dynamic, flower like-MoS2 nanosheets were prepared by hydrothermal method, and its antioxidant enzyme-mimic activities were assessed via electron spin resonance (ESR) spectroscopy. It was shown that MoS2 nanosheets had strong scavenging ability for hydroxyl radical (·OH) and singlet reactive oxygen species (1O2) in a dose-dependent manner. Using an in vitro lipopolysaccharide (LPS)-induced vascular endothelial cell injury model, the protective roles of MoS2 nanozyme on cytotoxicity and apoptosis of endothelial cells were examined by MTT and Annexin V-FITC/PI assay, respectively. Mitochondrial fission/fusion of endothelial cell were observed by Mito-Tracker green probe. Reactive oxygen species (ROS) probe DCFH-DA and superoxide anion probe DHE were used to detect the level of oxidative stress in vitro. Plasmid GFP-LC3 transfection using colocalization analysis was applied to assess the autophagy of endothelial cells. The results showed that MoS2 nanozyme could significantly reduce the cytotoxicity and apoptosis of endothelial cells stimulated by LPS, and prevent the impairment mitochondrial dynamics of endothelial cells, thus maintaining mitochondrial dynamics. In addition, MoS2 nanozyme was also shown to alleviate LPS-mediated endothelial mitochondrial autophagy, thus protecting endothelial cells from inflammatory stress. These results established that MoS2 nanozyme protected endothelial cells injury from inflammatory stress by regulating mitochondrial dynamics and mitochondrial autophagy of endothelial cells, which is expected to expand the use of MoS2 nanozyme in the prevention and treatment of inflammation-related vascular endothelial diseases.
