Fig. 6.
Fig. 6. Coadministration of paclitaxel and bryostatin 1 results in potentiation of TNF-α mRNA levels and prolonged protein accumulation. / U937 cells were treated with paclitaxel (5 nM) with or without bryostatin 1 (10 nM) for 3 hours (A) and 6 hours (B). Total RNA was isolated, and TNF-α mRNA expression was determined by RT-PCR as described in “Materials and methods.” U937 cells (C) and HL-60 cells (D) were treated with paclitaxel (10 nM) with or without bryostatin 1 (10 nM). The amount of TNF-α protein in the media was monitored at various time intervals (0 to 24 hours) by ELISA assay as described in “Materials and methods.” TNF-α protein is expressed as fold increase, reflected by changes in optical density, relative to untreated control cells. Results are representative of 3 separate experiments (means ± SE). *Significantly greater than the sum of the effects of each agent administered alone (P < .01).

Coadministration of paclitaxel and bryostatin 1 results in potentiation of TNF-α mRNA levels and prolonged protein accumulation.

U937 cells were treated with paclitaxel (5 nM) with or without bryostatin 1 (10 nM) for 3 hours (A) and 6 hours (B). Total RNA was isolated, and TNF-α mRNA expression was determined by RT-PCR as described in “Materials and methods.” U937 cells (C) and HL-60 cells (D) were treated with paclitaxel (10 nM) with or without bryostatin 1 (10 nM). The amount of TNF-α protein in the media was monitored at various time intervals (0 to 24 hours) by ELISA assay as described in “Materials and methods.” TNF-α protein is expressed as fold increase, reflected by changes in optical density, relative to untreated control cells. Results are representative of 3 separate experiments (means ± SE). *Significantly greater than the sum of the effects of each agent administered alone (P < .01).

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