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Fangchinoline, an Extract of the Stephania tetrandra S. Moore Root, Promoted Oxidative Stress-induced DNA Damage and Apoptosis and Inhibited Akt Signaling in Jurkat T Cells

Authors :
Shao, Yanxiong
Li, Chaoran
Miao, Guojun
Xu, Yubo
Source :
Current Molecular Pharmacology; 2024, Vol. 17 Issue: 1 p1-11, 11p
Publication Year :
2024

Abstract

Background: Fangchinoline (Fan) is extracted from traditional Chinese medicine (called Fangji), or the root of Stephania tetrandra Moore. Fangji is well-known in Chinese medical literature for treating rheumatic diseases. Sjogren's syndrome (SS) is a rheumatic disease whose progression can be mediated via CD4+ T cell infiltration.Objective: This study identifies the potential role of Fan in inducing apoptosis in Jurkat T cells.Methods: First, we explored the biological process (BP) associated with SS development by performing a gene ontology analysis of SS salivary gland-related mRNA microarray data. The effect of Fan on Jurkat cells was investigated by analyzing the viability, proliferation, apoptosis, reactive oxygen species (ROS) production, and DNA damage.Results: Biological process analysis showed that T cells played a role in salivary gland lesions in patients with SS, indicating the significance of T cell inhibition in SS treatment. Viability assays revealed that the half-maximal inhibitory concentration of Fan was 2.49 µM in Jurkat T cells, while the proliferation assay revealed that Fan had an inhibitory effect on the proliferation of Jurkat T cells. The results of the apoptotic, ROS, agarose gel electrophoresis, and immunofluorescence assays showed that Fan induced oxidative stress-induced apoptosis and DNA damage in a dosedependent manner.Conclusion: These results indicate that Fan could significantly induce oxidative stress-induced apoptosis and DNA damage and inhibit the proliferation of Jurkat T cells. Moreover, Fan further enhanced the inhibitory effect on DNA damage and apoptosis by inhibiting the pro-survival Akt signal.

Details

Language :
English
ISSN :
18744672 and 18744702
Volume :
17
Issue :
1
Database :
Supplemental Index
Journal :
Current Molecular Pharmacology
Publication Type :
Periodical
Accession number :
ejs66478786
Full Text :
https://doi.org/10.2174/1874467216666230210152454