It has been widely established that, in addition to its role in reproduction, progesterone (P4) also has potent anti-inflammatory effects. While the precise mechanisms have never been clearly elucidated in RAW 246.7 cells, it seems logical to assume that this response is – at least in part - a consequence of activation of and signaling through the progesterone receptor (P4-R). However, it has recently been shown that in a rat model, this anti-inflammatory effect is – in fact - independent of the progesterone receptor. In this project, the aim was to characterize this response by assaying nitric oxide production from lipopolysaccharide-challenged RAW 264.7 cells and ascertain the involvement of the P4-R. To determine the contribution of the receptor, RAW cells were incubated in the presence and absence of RU-486 – a potent P4-R antagonist. Our results indicate that the anti-inflammatory response of progesterone was in fact through the activation of the P4-R as cells incubated in RU-486 show an approximate 60% reversal of the inhibitory effect of P4 as compared to cells incubated in the absence of the antagonist. However, because we did not observe a complete reversal, suggests that perhaps other receptors come into play which will be addressed in future studies.

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