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Dihydromyricetin is a potent inhibitor with an IC50 of 48 μM on dihydropyrimidinase. Dihydromyricetin can activate autophagy through inhibiting mTOR signaling. Dihydromyricetin suppresses the formation of mTOR complexes (mTORC1/2).

Dihydromyricetin, a flavonol, significantly inhibits the catalytic activities of dihydropyrimidinase toward both the natural substrate dihydrouracil and xenobiotic substrate 5-propyl-hydantoin. Dihydromyricetin exhibits a significant inhibitory effect on the activities of dihydropyrimidinase for both substrates, even more than Myricetin does. The IC50 values of Dihydromyricetin for dihydropyrimidinase determined from the titration curves using Dihydrouracil and 5-propyl-hydantoin are 48±2 and 40±2 μM, respectively[1]. Dihydromyricetin (DHM) supplementation significantly reverses the increased phosphorylation of mTOR at Ser2448 (p-mTOR) during D-gal administration, which suggests that Dihydromyricetin can activate autophagy through inhibiting mTOR signaling[2].

Changes in learning and memory capacity in rats administrated normal control group, D-gal group, D-gal+Dihydromyricetin (100 mg/kg) group, D-gal+Dihydromyricetin (200 mg/kg) group assessed by morris water maze (MWM) (n=10 per group). Dihydromyricetin (DHM) treatment significantly shortens the escape latency when compared with D-gal-induced model group[2].

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