3-n-butylphthalide antagonizes etoposide-induced senescence in vascular endothelial cells
10.3969/j.issn.1009-0126.2024.03.021
- VernacularTitle:丁苯酞拮抗依托泊苷诱导的血管内皮细胞衰老
- Author:
Lingwei ZHAO
1
;
Zhouheng YE
;
Long CHENG
;
Xin LIU
;
Lei HAN
Author Information
1. 510641 广州,华南理工大学医学院
- Keywords:
etoposide;
human umbilical vein endothelial cells;
beta-galactosidase;
senescence-associ-ated secretory phenotype;
butylphthalide
- From:
Chinese Journal of Geriatric Heart Brain and Vessel Diseases
2024;26(3):327-330
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of 3-n-butylphthalide(NBP)on etoposide-induced senescence in human umbilical vein endothelial cells(HUVECs).Methods HUVECs were divid-ed into blank control group,etoposide group(500 nmol/L etoposide+dimethyl sulfoxide),etopo-side+low-,medium-and high-dose NBP groups(500 nmol/L etoposide+5,10 and 20 μmol/L NBP,respectively).Senescence-related β galactosidase(SA-β-gal)staining was used to observe the change in senescent cell proportion.Real-time quantitative PCR was employed to detect the mRNA levels of senescence-associated secretory phenotype(SASP),such as IL-8,IL-1β,and CXC chemokine ligand 1(CXCL1).Western blotting was applied to measure the expression level of ag-ing-related protein,P21.Immunofluorescence staining was utilized to detect the proportion of pro-liferation-related protein Ki67 positive cells.Results Significantly higher P21 expression(1.00± 0.00 vs 0.59±0.09),larger ratio of SA-β-gal positive cells(29.58±4.51)％vs(11.27±1.18)％,increased mRNA levels of IL-8(2.49±0.11 vs 1.00±0.03),IL-1β(6.32±0.15 vs 1.00±0.03)and CXCL1(2.40±0.24 vs 1.00±0.04),but reduced proportion of Ki67 positive cells(5.95±1.55)％vs(27.38±7.00)％were observed in the etoposide group than the blank control group(P＜0.05).Low-dose NBP treatment decreased the ratio of SA-β-gal positive cells,P21 protein level,and mRNA level of IL-1β,and increased the proportion of Ki67 positive cells when compared with the etoposide group(P＜0.05).Conclusion NBP has an antagonistic effect on etoposide-induced se-nescence of vascular endothelial cells.
