中国药科大学学报2025，Vol.56Issue(2)：216-224,9.DOI:10.11665/j.issn.1000-5048.2024091403
银杏内酯B通过PI3K/AKT信号通路抑制MH7A人成纤维样滑膜细胞增殖及其促细胞凋亡
Ginkgolide B inhibits cell proliferation and promotes cell apoptosis of MH7A human fibroblast-like synoviocytes through PI3K/AKT pathway
摘要
Abstract
To explore the inhibitory effect of ginkgolide B(GB)on MH7A human fibroblast-like synoviocytes(FLS)and its potential mechanism.Firstly,20 μg/L tumor necrosis factor-α(TNF-α)was pretreated with MH7A to establish a cell model of arthritis.After incubation of MH7A cells with various concentrations of GB,CCK-8 assay,Transwell assay,and flow cytometry(FCM)were separately used to detect cell viability,cell invasion,and cell apoptosis rate and cell cycle;Real-time quantitative PCR and Western blot assay were performed to detect the apoptosis-and cycle-related gene transcriptions and protein expressions,respectively.The results showed that compared with the control group,GB dose-and time-dependently suppressed cell viability to a greater extent;GB significantly reduced cell invasive ability and increased cell apoptosis rate and proportion of G0/G1 phase in MH7A cells,along with increased transcription levels of Bcl-2-associated X protein(Bax)and p21 mRNA and decreased transcription levels of Bcl-2,myeloid cell leukemia 1(Mcl-1),protein kinase B(PKB;AKT),IP3K,Cyclin D1 and cyclin-dependent kinase 4(CDK4)mRNA;GB remarkably increased expression levels of Bax,p21,and cleaved-Caspase 3 protein and decreased expression levels of Bcl-2,Mcl-1,p-AKT,p-PI3K,Cyclin D1,and CDK4 protein,with decreased ratios of p-PI3K/PI3K,p-AKT/AKT,and Bcl-2/Bax.In conclusion,GB blocks the G1-to-S cell cycle transition,suppresses cell viability and cell invasion and induces cell apoptosis of MH7A human RA-FLS via suppressing the PI3K/AKT signaling pathway.关键词
银杏内酯B/磷脂酰肌醇3-激酶/蛋白激酶B/类风湿性关节炎/MH7A细胞/凋亡Key words
ginkgolide B/PI3K/AKT/rheumatoid arthritis/MH7A cell/cell apoptosis分类
医药卫生引用本文复制引用
刘璘琛,徐晓龑,孙春萌,俞济荣,施青,孙君君,逄丹丹,卫斐然,刘兴..银杏内酯B通过PI3K/AKT信号通路抑制MH7A人成纤维样滑膜细胞增殖及其促细胞凋亡[J].中国药科大学学报,2025,56(2):216-224,9.基金项目
国家自然科学基金项目(No.22278442) This study was supported by the National Natural Science Foundation of China(No.22278442) （No.22278442）
