Research on the inhibitory effects of evodiamine on activated T cell proliferation.
- Author:
Jianan TANG
1
;
Xingyan LUO
2
;
Jingjing HE
1
;
Xiaoxin ZENG
3
;
Yang LIU
2
;
Yi LAI
4
,
5
Author Information
1. School of Clinical Medicine, Chengdu Medical College, Chengdu 610500, China.
2. Center for Scientific Research, Chengdu Medical College, Chengdu 610500, China.
3. School of Laboratory Medicine, Chengdu Medical College, Chengdu 610500, China.
4. School of Laboratory Medicine, Chengdu Medical College, Chengdu 610500, China. *Corresponding author, E-mail: sculy926@
5. com.
- Publication Type:Journal Article
- MeSH:
Humans;
Cell Proliferation/drug effects*;
Quinazolines/pharmacology*;
T-Lymphocytes/metabolism*;
Lymphocyte Activation/drug effects*;
Apoptosis/drug effects*;
Interleukin-4/metabolism*;
Interleukin-10/metabolism*;
Interleukin-2 Receptor alpha Subunit/metabolism*;
Interleukin-17/metabolism*;
Interleukin-2/metabolism*;
Cell Cycle/drug effects*;
Cells, Cultured
- From:
Chinese Journal of Cellular and Molecular Immunology
2025;41(6):524-530
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the characteristics of the inhibitory effect of Evodiamine on the proliferation of activated T cells. Methods Mononuclear cells from peripheral blood (PBMCs) were obtained from healthy donors through density gradient centrifugation, and T cells were subsequently purified by using immunomagnetic bead separation. T cell activation was induced by employing anti-human CD3 and anti-human CD28 antibodies. T cells were treated with different concentrations of EVO (0.37, 1.11, 3.33, and 10)μmol/L. Flow cytometry was applied to evaluate the proliferation index, apoptosis rate, viability, CD25 expression levels, and cell cycle distribution of T cells. The expression levels of cytokines IL-2, IL-17A, IL-4, and IL-10 were quantified by using ELISA. Results 1.11, 3.33 and 10 μmol/L EVO effectively inhibited the proliferation of activated T cells, with an IC50 of (1.5±0.3)μmol/L. EVO did not induce apoptosis in activated T cells and affect the survival rate of resting T cells. EVO did not affect the expression of CD25 and the secretion of IL-2 in activated T cells. EVO arrested the T cell cycle at the G2/M phase, resulting in an increase in G2/M phase cells, and exhibited a concentration-dependent effect. EVO did not affect the secretion of IL-4, IL-10 by activated T cells, but significantly inhibited the secretion of IL-17A. Conclusion EVO did not significantly affect the activation process of T cells but inhibited T cell proliferation by arresting the cell cycle at the G2/M phase and significantly suppressed the secretion of the pro-inflammatory cytokine IL-17A, which suggests that EVO has the potential to serve as a lead compound for the development of low-toxicity and high-efficiency immunosuppressants and elucidates the mechanisms underlying the anti-inflammatory and immunomodulatory effects of the traditional Chinese medicine Evodia rutaecarpa.
