Salvia miltiorrhiza-derived exosome-like nanoparticles attenuate oxidative damage of vascular endothelial cells via PI3K/Akt/eNOS signaling pathway
10.3969/j.issn.1000-4718.2025.10.003
- VernacularTitle:丹参衍生的外泌体样纳米颗粒通过PI3K/Akt/eNOS信号通路减轻血管内皮细胞氧化损伤
- Author:
Xiaoyong HU
1
;
Zhaoying YANG
1
;
Qianhua SONG
1
;
Zhongying LÜ
1
;
Rui TANG
1
;
Huan WANG
1
;
Hongjian LI
1
Author Information
1. 新疆医科大学第五临床医学院高血压科,新疆 乌鲁木齐 830011
- Publication Type:Journal Article
- Keywords:
Salvia miltiorrhiza;
exosomes;
nanoparticles;
vascular endothelial cells;
oxidative damage;
PI3K/Akt/eNOS signaling pathway
- From:
Chinese Journal of Pathophysiology
2025;41(10):1892-1899
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To explore the mechanism of Salvia miltiorrhiza(Danshen)-derived exosome-like nanoparti-cles(DDN)in attenuating oxidative damage in endothelial cells through the activation of the phosphatidylinositol 3-kinase(PI3K)/protein kinase B(PKB/Akt)/endothelial nitric oxide synthase(eNOS)signaling pathway.METHODS:The DDN were characterized by transmission electron microscopy and dynamic light scattering.Fluorescence microscopy and flow cytometry were used to evaluate the uptake of DDN by human umbilical vein endothelial cells(HUVECs).The viability,migration and invasion of HUVECs were assessed using CCK8 assay,wound-healing assay and Transwell assay,respec-tively.The HUVECs were induced by angiotensin II(Ang II)for oxidative stress and intervened with DDN or LY294002(a PI3K inhibitor).The levels of reactive oxygen species were determined by flow cytometry,and intracellular nitric oxide(NO)content was measured using a biochemical assay kit.Additionally,the protein levels of NADPH oxidase 4(NOX4),NOX2,endothelial nitric oxide syntnase(eNOS),p-eNOS,Akt and p-Akt were examined by Western blot.RESULTS:(1)Transmission electron microscopy and dynamic light scattering analysis revealed that DDN had good bio-compatibility and stability.(2)According to fluorescence images and flow cytometry results,DDN were strongly taken up by HUVECs.(3)Compared with control group,DDN significantly promoted the viability,migration and invasion of HUVECs,showing a dose-dependent effect.(4)Compared with control group,DDN remarkably increased intracellular NO levels,thereby enhancing endothelial cell vasodilation via activating the PI3K/Akt/eNOS signaling pathway.(5)The PI3K/Akt/eNOS pathway played a critical role in mitigating oxidative stress and improving cellular function in response to DDN treat-ment.CONCLUSION:The DDN mediate PI3K/Akt/eNOS signaling pathway activation to significantly alleviate Ang II-induced oxidative damage in endothelial cells,suggesting a potential vascular protective effect of DDN.
