Genistein Reverses Diminished T-Cell Signal Transduction, Induced by Post-Menopausal Estrogen Levels

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This study addressed the ability of genistein to reverse the loss of T-cell signaling components, induced by estrogen deficiency associated with aging.

Method of study

Using Jurkat 6.1 T cells, genistein regulation of CD3ζ, JAK3, and NFκB was analysed by Western immunoblotting at 4 or 40 pg/mL (post- and pre-menopausal levels, respectively) estradiol (E2). Corresponding gene expressions were quantified by real-time polymerase chain reaction (RT-PCR). For functionality, levels of IL-2 were correlated with its transcription by RT-PCR.


At 4 pg/mL E2, signaling proteins were decreased compared with 40 pg/mL: CD3ζ, 1.58-fold; JAK3, 1.75-fold; and NFκB, 1.73-fold (P < 0.001). Genistein, at 0.5 and 5.0 μM, added to 4 pg/mL E2 induced their expression to 40 pg/mL levels. While significantly diminished IL-2 mRNA levels were observed at 4 pg/mL E2, genistein induced IL-2 mRNA to 40 pg/mL levels.


Genistein restores CD3ζ, NFκB and JAK3 proteins and mRNAs at post-meonopausal estrogen levels, in vitro, with no significant effect at pre-menopausal estrogen levels.

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