Methysticin, a major kavalactone extracted from kava, can induce CYP1A1.

Methysticin triggers the most profound inducing effect on CYP1A1. Methysticin is able to activate the AhR signaling pathway. Hepa1c1c7 cells are treated with various concentrations of kava extract (0-50 μg/mL) and six kavalactones (0-100 μM) for 24 h. The results indicate that kava extract at concentrations up to 50 μg/mL and kavalactones up to 100 μM do not induce cell death. For the following studies, kava extract at 0.78-6.25 μg/mL and kavalactones at 0.78-25 μM, concentrations that cause no damage to cells, are used [1].

Methysticin (6 mg/kg) is administered once a week for a period of 6 months to 6-month-old transgenic APP/Psen1 mice by oral gavage. Methysticin treatment activates the Nrf2 pathway in the hippocampus and cortex of mice. The Aβ deposition in brains of Methysticin-treated APP/Psen1 mice is not altered compared to untreated mice. However, Methysticin treatment significantly reduces microgliosis, astrogliosis, and secretion of the pro-inflammatory cytokines TNF-α and IL-17A. Methysticin treatment results in significant activation of the Nrf2/ARE pathway in the hippocampus and the cortex but not in the midbrain and cerebellum of ARE-luciferase reporter gene mice. Methysticin treatment significantly increases the expression of both genes compared to untreated animals [2].

20697-20-5

C15H14O5

274.27

(±)-Methystici;麻醉椒苦素;DL-Methysticin

Ethanol:1 mg/mL (3.65 mM)
DMSO:5 mg/mL (18.23 mM)
Powder: -20°C for 3 years
In solvent: -80°C for 2 years