Hypaconitine (HA), an active and highly toxic constituent derived from Aconitum species, is widely used to treat rheumatism. Little is known about the hepatic cytochrome P450-catalyzed metabolism of HA. The present study investigated the metabolism of HA in vitro using male human liver microsomes (MHLMS). The results of chemical inhibition, monoclonal antibody inhibition, and cDNA-expressed CYP enzyme studies showed that the primary contributors toward HA metabolism were CYP3A4 and 3A5, with secondary contributions by CYP2C19, 2D6, and CYP2E1. CYP1A2 and 2C8 provided minor contributions.
|Product Name||Aconite Root Extract|
|Storage Condition||Store in cool & dry place, Keep away from strong light and heat.|
Loss on Dring
1. Hypaconitine (HA), an active and highly toxic constituent derived from Aconitum species, is widely used to treat rheumatism, the hepatic cytochrome P450-catalyzed metabolism of HA.
2. Hypaconitine and aconitine produce neuromuscular blockade by reducing the evoked quantal release, the mechanism of this effect was attributed mainly to blocking of the nerve compound action potential.
3. Hypaconitine induces QT prolongation, mediated through inhibition of KCNH2 (hERG) potassium channels in conscious dogs.
4. Hypaconitine has anti-inflammatory activity.
5. Hypaconitine can inhibit CaM expression and Cx43 (Ser368) phosphorylation, and liquiritin can interfere with this kind of effect by synergistically inhibiting CaM expression and by antagonizing Cx43 (Ser368) dephosphorylation induced by hypaconitine.