Ginkgolide B inhibits cell proliferation and promotes cell apoptosis of MH7A human fibroblast-like synoviocytes through PI3K/AKT pathway
10.11665/j.issn.1000-5048.2024091403
- VernacularTitle: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
- Author:
Linchen LIU
1
,
2
,
3
;
Xiaoyan XU
;
Chunmeng WEI
;
Jirong YU
;
Qing SHI
;
Junjun SUN
;
Dandan PANG
;
Feiran WEI
;
Xing LIU
Author Information
1. 东南大学附属中大医院风湿科, 南京210009
2. 中国药科大学药学院药剂系, 南京210009
3. 东南大学医学院, 南京210009
- Publication Type:Journal Article
- Keywords:
ginkgolide B;
PI3K/AKT;
rheumatoid arthritis;
MH7A cell;
cell apoptosis
- From:
Journal of China Pharmaceutical University
2025;56(2):216-224
- CountryChina
- Language:Chinese
-
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.
