- Author:
Guang ZENG
1
;
Jiang CHEN
;
Qing-Hua LIANG
;
Wan-Hui YOU
;
Han-Jun WU
;
Xin-Gui XIONG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cell Nucleus; drug effects; metabolism; Cell Proliferation; drug effects; I-kappa B Proteins; metabolism; Interleukin-2; secretion; Ionomycin; pharmacology; Lymphocyte Activation; drug effects; Mice; Mice, Inbred BALB C; NF-KappaB Inhibitor alpha; NF-kappa B; metabolism; Phosphorylation; drug effects; Protein Transport; drug effects; Signal Transduction; drug effects; T-Lymphocytes; cytology; drug effects; immunology; secretion; Tetradecanoylphorbol Acetate; pharmacology; Triterpenes; pharmacology
- From: Chinese journal of integrative medicine 2012;18(1):34-39
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo investigate the effects of ursolic acid (UA) on T-cell proliferation and activation, as well as to examine its effect on nuclear factor-κB (NF-κB) signaling pathway in T cells.
METHODST-cells isolated from BALB/c mice were incubated with UA at concentrations ranging from 5-30 μmol/L in the presence of phorbol 12-myristate 13-acetate (PMA) or PMA plus ionomycin. The proliferation of T cells was measured by the MTT assay. The expressions of CD69, CD25, and CD71 on T-cell surface were analyzed using flow cytometry. The level of interleukin-2 (IL-2) in the culture supernatant of activated T cells was quantified by enzyme-linked immunosorbent assay (ELISA). The level of phosphorylated IκB-α (p-IκB-α) in total protein and p65, a subunit of NF-κB, nuclear translocation were measured by Western blot analysis.
RESULTSUA in a dose-dependent manner significantly decreased the proliferation and inhibited the surface expressions of CD69, CD25, and CD71 in murine T lymphocytes upon in vitro activation (P<0.01). Significant reduction of IL-2 production was found in activated T cells treated with UA (P<0.01). The PMA-induced increase in p-IκB-α protein was inhibited, and nuclear translocation of p65 from the cytoplasm was blocked by UA.
CONCLUSIONUA is a potent inhibitor for T cell activation and proliferation; these effects are associated with the inhibition of NF-κB signaling pathway.