4 research outputs found

    The effect of p38 MAPK blockade on etoposide, 5-FU, and doxorubicin mediated induction of inflammatory cytokine production in murine macrophages.

    No full text
    <p>(A) Inhibition of p38 MAPK leads to a reduction in MAPKAPK-2 phosphorylation , a downstream target of p38 MAPK. (B) The effect of pre-treatment with the p38 MAPK inhibitor on IL-1β, TNF-α and IL-6 mRNA levels. Fold increase in expression of each cytokine mRNA in drug treated cells and in cells treated with drug plus inhibitor relative to carrier treated cells is shown. (C) Levels of IL-1β, TNF-α and IL-6 in the culture supernatant of drug treated cells. A significant decrease (p<0.05) in cytokine level in cells treated with drug plus p38 MAPK inhibitor relative to cells treated with drug alone is denoted by an asterisk.</p

    The cytotoxic effects of etoposide, 5-fluorouracil, doxorubicin, and docetaxel are not associated with p38 MAPK activation in LLC11 cells.

    No full text
    <p>A) The effect of increasing concentrations of etoposide, 5-FU, doxorubicin or docetaxel on p38 MAPK activation and proliferation were assessed by immunoblotting and MTS assay respectively. B) The effect of p38 MAPK blockade on drug-induced cytotoxicity in LLC1 cells treated with etoposide, 5-FU or doxorubicin. Note that the addition of the p38 MAPK inhibitor appeared to enhance the cytotoxic effects of 5-FU on LLC1 cells (see *).</p

    Additive effects of 1R-Chl and imatinib treatments.

    No full text
    <p>(A) Murine BM cells transduced with unmutated BCR-ABL were treated with 500 nM imatinib, 500 nM 1R-Chl, and 500 nM 1S-Chl individually, or in combination of either 500 nM 1R-Chl or 500 nM 1S-Chl with 500 nM imatinib. (B) Same treatment routines were used on CML patient MNCs. The CML patient MNCs were treated 500 nM imatinib, 500 nM 1R-Chl, and 500 nM 1S-Chl individually, or 500 nM 1R(S)-Chl in combination with 500 nM imatinib. (C) Same experiments were done on normal blood donor MNCs.</p
    corecore