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Both agonists were able to significantly induce the expression of megalin in BN and in LLC-PK1 cells.
Both agonists were able to enhance NO production, and this effect was abolished when ERα was antagonized by Fulvestrant (Figure 2B).
Interestingly, when the cells were treated with PPAR agonists and BSA (10 mg/ml) simultaneously, both agonists were able to significantly counteract the inhibitory effect of BSA on megalin expression.
Moreover, both agonists were able to downregulate the gene expression of potential chemokines in cultured rat hepatocytes.
Similar(56)
For example, both agonists are able to activate PLC-dependent pathways.
Thus, these results suggest that E2 and both ER agonists were able to limit T/HS-induced morphologic gut injury and prevent bacterial translocation.
Subsequently, both PPARgamma agonists were able to attenuate macrophage infiltration into AT, measured by the reduction of MCP1 and F4/80 expression.
In their experiments, both EP2- and EP4-selective agonists were able to mimic these effects.
The classical D2DR agonists were able to negatively modulate both A2AAR affinity and functionality.
However, none of the tested agonists were able to elicit a signal above the CCh response.
Seven out of the ten agonists were able to stimulate the calcium signal at 1-40 μM concentrations of crude extract.
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