Gomisin A from the fruit of Schisandra chinensis has many pharmacological properties, including hepato-protective, anti-diabetic, and anti-oxidative stress. Gomisin A inhibited reactive oxygen species production even in the SIPS-HDF (stress-induced premature senescence-human diploid fibroblast) cells. Gomisin A was also able to attenuate the activity of senescence-associated β-galactosidase and the production of pro-inflammatory molecules in the SIPS as well as aged HDF cells. In addition, gomisin A promoted the autophagy and mitochondrial biogenesis factors through the translocation of nuclear factor erythroid 2-related factor-2, and inhibited aging progression in the SIPS-HDF cells[3]. Using human liver microsomes, a reversible inhibition assay revealed that Gom A ( Gomisin A) was a competitive inhibitor with a KI value of 1.10 µM, and the time- and NADPH-dependent CYP3A inhibition of Gom A was observed in a time-dependent inhibition assay (KI = 0.35 µM, kinact = 1.96 min-1)[4]. Both oral and intraperitoneal administration of G.A (50 mg/kg) inhibited lung metastasis of CT26 cells. G.A (Gomisin A) significantly decreased the viability of various CRC (colorectal cancer) cell lines, whereas it did not change the proliferation of normal colon cells. Moreover, the migration and invasion of CRC cells were reduced by G.A treatment. Especially, G.A decreased matrix metalloproteinase (MMP)-2 and MMP-9 expressions and activities[5].
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