Mogrol is a biometabolite of mogrosides, and acts via inhibition of the ERK1/2 and STAT3 pathways, or reducing CREB activation and activating AMPK signaling.
In Vitro
Mogrol (0-250 µM) significantly and dose- and time-dependently inhibits K562 cell growth and increases the number of apoptotic cells. Mogrol (0, 10, 100, and 250 µM) induces G1 phase cell cycle arrest in K562 cells. Treatment with mogrol significantly decreases ERK phosphorylation as compared to control cells, whereas total ERK protein is not affected. Mogrol dose-dependently induces growth arrest in G0/G1 phase of the cell cycle. Mogrol significantly and dose-dependently enhances p21 protein expression in K562 cells. Mogrol significantly represses the increase in cellular TG levels induced by differentiation stimuli, and suppresses TG accumulation at micromolar levels, with a statistically significant suppression observed above 10 μM. Mogrol suppresses adipogenesis in 3T3-L1 cells at concentrations that does not affect cell viability. Mogrol suppresses adipogenesis through at least two different mechanisms, increasing AMPK phosphorylation and repressing the activation of CREB. MCE has not independently confirmed the accuracy of these methods. They are for reference only.
