Fig. 3. Effects of H89, a cyclic adenosine 3′,5′-monophosphate-dependent protein kinase inhibitor, on the proopiomelanocortin gene expression. In the presence or absence of 30 μm H89, cells were treated with 10 μm diazepam or 10 μm midazolam, and stimulated with 1 μm corticotropin-releasing hormone (CRH). The ratios of luciferase activity to that of nonstimulated control cells are expressed as means ± SD from seven experiments. *P < 0.05 versus  cells stimulated with CRH without H89. #P < 0.05 versus  cells stimulated with CRH without benzodiazepines and H89.

Fig. 3. Effects of H89, a cyclic adenosine 3′,5′-monophosphate-dependent protein kinase inhibitor, on the proopiomelanocortin gene expression. In the presence or absence of 30 μm H89, cells were treated with 10 μm diazepam or 10 μm midazolam, and stimulated with 1 μm corticotropin-releasing hormone (CRH). The ratios of luciferase activity to that of nonstimulated control cells are expressed as means ± SD from seven experiments. *P < 0.05 versus  cells stimulated with CRH without H89. #P < 0.05 versus  cells stimulated with CRH without benzodiazepines and H89.

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