Title: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
Volume: 17
Author(s): Yanxiong Shao, Chaoran Li, Guojun Miao and Yubo Xu*
Affiliation:
- Department of Stomatology, Shanghai East Hospital, School of Medicine, Tongji University, Jimo Road 150, Shanghai 200092, China
Keywords:
Fangchinoline, Reactive, Oxygen species, DNA damage, Apoptosis, Akt.
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.