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Similarly, TGR5 activation elevates intracellular cAMP levels, leading to downstream activation of protein kinase A (PKA) and exchange protein directly activated by cAMP (Epac), which suppresses NF-B signaling, inhibits NLRP3 inflammasome activation, and can promote macrophage polarization from the pro-inflammatory M1 phenotype toward the anti-inflammatory M2 phenotype 148

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This approach has significant potential, given the unique vulnerability of cancer cells to oxidative stressa characteristic that can be exploited for therapeutic benefit