Mechanism of abnormal function and inflammatory response of HUVEC induced by Helicobacter pylori infection
10.3969/j.issn.1009-0126.2024.02.019
- VernacularTitle:幽门螺杆菌感染所致人脐静脉内皮细胞功能异常及炎性反应的作用机制研究
- Author:
Jing SUN
1
;
Shihe SHAO
;
Jiaxin XUE
;
Huazi ZHU
;
Chen SHAO
Author Information
1. 212000 镇江,江苏大学附属医院心内科
- Keywords:
Helicobacter pylori;
human umbilical vein endothelial cells;
STAT3/nuclear factor κB pathway;
apoptosis;
cell proliferation
- From:
Chinese Journal of Geriatric Heart Brain and Vessel Diseases
2024;26(2):197-201
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of Helicobacter pylori(Hp)on the proliferation,migration,apoptosis and inflammatory response of human umbilical vein endothelial cells(HUVEC)through activation of STAT3/nuclear factor κB(NF-κB)pathway.Methods HUVEC were divided into control group(without Hp infection)and Hp group(multiplicity of infection=25).Cell morphology was observed with inverted microscopy,proliferation was detected by CCK-8 assay and plate cloning assay,and the migration ability was examined by Transwell migration as-say and wound healing assay.Flow cytometry was used to detect the apoptotic rate.Real-time fluo-rescence quantitative PCR was employed to measure the mRNA expression of cytotoxin-associat-ed gene A(CagA),IL-6,IL-8,IL-1β and TNF-α.Western blotting was applied to determine the protein expression of Cyclin D1,proto-oncogene C-Myc,MMP-2,MMP-9,PCNA,Bax,Bcl-2 and STAT3/NF-κB signaling pathway.Results Hp infection resulted in suppressed proliferation and migration abilities,decreased protein levels of Cyclin D1,PCNA,C-Myc,MMP-2,MMP-9 and Bcl-2,elevated protein levels of Bax,p-STAT3/STAT3,p-NF-KB p65/NF-κB p65,raised apoptotic rate,and significantly increased mRNA levels of IL-6,IL-8,IL-1β and TNF-α(2.71±0.05 vs 1.06±0.41,1.42±0.02 vs 0.92±0.11,2.50±0.29 vs 1.00±0.10,5.34±0.57 vs 1.00±0.16;P＜0.01)when compared with the control group.Conclusion Hp infection inhibits proliferation and migra-tion,and induces apoptosis and inflammatory response in HUVEC through activation of the STAT3/NF-κB pathway.
