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- W1828659332 abstract "A potent Nrf-2 activator sulforaphane (SF), which is currently under clinical trials for cancer therapy, was employed to elucidate the role of Keap1/Nrf-2/ARE signalling pathway in T-cell responses. SF suppressed mitogen induced T-cell and B-cell proliferation. It also inhibited mitogen induced upregulation of T-cell (CD25 and CD69) and B-cell (CD80 and CD86) activation markers and suppressed secretion of cytokines (IL-2, IL-4, IL-6 and IFN-γ). SF induced oxidative stress and its anti-inflammatory effects were abrogated by thiol antioxidants. SF activated PI3K/AKT, leading to phosphorylation mediated suppression of GSK3β resulting in Nrf-2 activation. We also show for the first time that SF can prevent direct interaction between NF-κB and its consensus sequence by modulating thiol groups. It also suppressed homeostatic proliferation of T-cells and suppressed lipopolysaccharide induced pro-inflammatory mediators in macrophages. Our study shows that the potent anti-inflammatory effects of SF are mediated via modulation of PI3K/AKT/GSK3β/Nrf-2 and NF-κB pathway in T-cells." @default.
- W1828659332 created "2016-06-24" @default.
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- W1828659332 date "2015-12-01" @default.
- W1828659332 modified "2023-09-30" @default.
- W1828659332 title "Sulforaphane, a naturally occurring isothiocyanate, exhibits anti-inflammatory effects by targeting GSK3β/Nrf-2 and NF-κB pathways in T cells" @default.
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- W1828659332 doi "https://doi.org/10.1016/j.jff.2015.08.030" @default.
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