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Smilax China L.Rhizome Extract Inhibits nuclear factor-κb and Induces Apoptosis in Ovarian Cancer Cells

Chinese Journal of Integrative Medicine 2015年第12期21卷 907-915页

作者：胡丽玲陈东生王燕燕秦铀黄璞于丽秀廖婧华小黎 The First College of Clinical Medical Science China Three Gorges University Department of Pharmacy Union HospitalTongji Medical CollegeHuazhong University of Science and Technology Department of Hematology Union HospitalTongji Medical CollegeHuazhong University of Science and Technology

Objective： To study the antitumor effects and associated mechanisms of extract of the Smilax china L. rhizome （SCR） on ovarian cancer cells. Methods： Ovarian cancer cells A2780 were treated with different concentrations of SCR extract （SCRE）, and compared with controls. Effects on cell growth were evaluated by cell counting kit-8 （CCK-8） assay; proliferation effects by EdU incorporation assay; cell cycle by propidium iodide staining; apoptosis by annexin V-fluorescein isothiocyanate/propidium iodide; cellular distribution of nuclear factor- κ b （NF-κ b） by immunofluorescence; protein levels of NF- κb, caspase-3, poly-adenosine diphosphate （ADP）-ribose polymerase （PARP）, bcl-2-associated X protein （bax）, cellular inhibitor of apoptosis （clAP）-1, anti-X-linked inhibitor of apoptosis protein （XlAP）, b-cell lymphoma-extra large （bcI-XL）, b-cell lymphoma-2 （bcl-2） and AKT by Western blotting; and effects of SCRE combined with cisplatin or adriamycin on A2780 cells by CCK-8 assay. Results： SCRE suppressed A2780 cell proliferation in a dose-dependent manner （P〈0.05, /=〈0.01）, arrested cells in GJM phase and induced apoptosis by activating caspase-3, PARP and bax. SCRE treatment also correlated with inhibition of NF-κ b and downregulation of bcl-2, bcl-XL, clAP-l, XlAP and AKT. SCRE can promote chemosensitivity to cisplatin and adriamycin in A2780 cells （P〈0.01）. Conclusion： SCR effectively inhibits NF- κ b, induces apoptosis and reduces chemoresistance to cisplatin and adriamycin in ovarian cancer cells, which might be its molecular basis for treating ovarian cancer.

关键词： Smilax china L. rhizome A2780 cells G2/M arrest apoptosis nuclear factor- κ b chemosensitivity

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Ursolic Acid Inhibits T-Cell Activation through Modulating nuclear factor-κb Signaling

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Chinese Journal of Integrative Medicine 2012年第1期18卷 34-39页

作者：曾光陈疆梁清华游万辉吴汉军熊新贵 Institute of Integrative Medicine Xiangya HospitalCentral South University Telemedicine Centre Xiangya HospitalCentral South University

Objective： To investigate the effects of ursolic acid （UA） on T-cell proliferation and activation, as well as to examine its effect on nuclear factor- κ b （NF- κ b） signaling pathway in T cells. Methods： T-cells isolated from bALb/c mice were incubated with UA at concentrations ranging from 5-30μmol/L in the presence of phorbol 12-myristate 13-acetate （PMA） or PMA plus ionomycin. The proliferation of T cells was measured by the MIF 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 I κ b-α （p-I κ b-α ） in total protein and p65, a subunit of NF- κ b, nuclear translocation were measured by Western blot analysis. Results： UA 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-I κ b-α protein was inhibited, and nuclear translocation of p65 from the cytoplasm was blocked by UA. Conclusion： UA is a potent inhibitor for T cell activation and proliferation; these effects are associated with the inhibition of NF- κ b signaling pathway.

关键词： ursolic acid T-cell activation CD69 CD25 CD71 nuclear factor- κ b

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