Wogonin, baicalein, scutellarein and baicalin (in reducing order of potency), which all contain a certain flavonoid phenylbenzopyrone nucleus, have been shown in vitro to bind with the benzodiazepine site of the GABA-A receptor (Hui et al 2000).
Oral administration of wogonin (7.5-30 mg/kg) has been shown to interact with GABA-A receptors and produce an anxiolytic response that was similar to diazepam in the elevated plus-maze. Unlike benzodiazepines, wogonin was able to reduce anxiety without causing sedation or myorelaxation (Hui et al 2002, Kwok et al 2002).
Baicalin (10 mg/kg IP) and balcalln (20 mg/kg IP) have also been shown In vivo to produce an anxiolytic effect, mediated through activation of the benzodiazepine binding sites of GABA-A receptors (Liao et al 2003).
Two other flavones, 5,7-dihydroxy-6-methoxyflavone (oroxylin A) and 5,7,2'-trihydroxy-6,8-dimethoxyflavone (K36), also act as antagonist at the GABA-A recognition site and have demonstrated anxiolytic activity in vivo (Huen et al 2003a, b).
A water-extract of baical skullcap demonstrated anticonvulsant activity against electroshock-induced tonic seizures in vivo. Interestingly, the authors suggest that the effect might not be via the activation of the benzodiazepine binding site of GABA-A receptors, but probably via the prevention of seizure spread (Liao et al 2003, Wang et al 2000).
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