Aspirin promotes apoptosis and inhibits proliferation by blocking G0/G1 into S phase in rheumatoid arthritis fibroblast-like synoviocytes via downregulation of JAK/STAT3 and NF-κB signaling pathway

International Journal of Molecular Medicine
Xiaoqi ZhangMinqi Li

Abstract

Rheumatoid arthritis (RA) is a commonly occurring autoimmune disease. Its defining pathological characteristic is the excessive proliferation of fibroblast‑like synoviocytes (FLS), which is similar to tumor cells and results in a range of clinical problems. As a commonly used antipyretic, analgesic and anti‑inflammatory drug, aspirin is the first‑line treatment for RA. However, its mechanism of action has not been well explained. The goal is to investigate the biological effects of aspirin on primary RA‑FLS and its underlying mechanisms. In this experiment we treated cells with various concentrations of aspirin (0, DMSO, 1, 2, 5, 10 mM). Cell proliferation activity was detected with CCK‑8 assays. Apoptosis and cell cycle distribution were detected via flow cytometry. Apoptosis and cell cycle‑associated proteins (Bcl‑2, Bax, PRAP1, Cyclin D1, P21), as well as the key proteins and their phosphorylation levels of the NF‑κB and JAK/STAT3 signaling pathways, were detected via western blot analysis. Bioinformatics prediction revealed that aspirin was closely associated with cell proliferation and apoptosis, including the p53 and NF‑κB signaling pathways. By stimulating with aspirin, cell viability decreased, while the proportion of a...Continue Reading

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Citations

Jul 2, 2020·Cancer Management and Research·Xiangjie FuPeijun Liu
Apr 2, 2021·Journal of Theoretical Biology·Muhammad Suleman AwanAfrose Liaquat

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Methods Mentioned

BETA
flow
Assay
flow cytometry

Software Mentioned

Database for Annotation Visualization and Integrated Discovery...
BD Accuri C6 Plus
SPSS
Cytoscape
Cytohubba

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