Galangin shows inhibition of CYP1A1 (cytochrome P450 1A1) activity. Galangin inhibited the catabolic breakdown of DMBA (7,12-dimethylbenz[a]anthracene), as measured by thin-layer chromatography, in a dose-dependent manner. Galangin also inhibited the formation of DMBA-DNA adducts, and prevented DMBA-induced inhibition of cell growth. Moreover, galangin is a potent inhibitor of DMBA metabolism and an agonist/antagonist of the AhR[3]. Galangin treatment inhibited cell proliferation and induced autophagy (130 μ mol/l) and apoptosis (370 μ mol/l). The galangin-induced autophagy was attenuated by the inhibition of p53 in HepG2 cells, and overexpression of p53 in Hep3B cells restored the galangin-induced higher percentage of cells with vacuoles to normal level[4]. Galangin prevents HCC through multiple anti-cancer mechanisms, anti-genotoxic activity against environmental and dietary carcinogens; anti-proliferative effects through reversal of the Warburg effect in HCC(Hepatocellular carcinoma); arrest of the cell cycle in the G0/G1 phase; induction of apoptosis via stimulation of reactive oxygen species (ROS), endoplasmic reticulum (ER) stress, and the mitochondrial-dependent apoptosis pathway; induction of autophagy; and inhibition of angiogenesis, metastasis, and multidrug resistance (MDR) [5].
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