Many in vitro and in vivo trials have demonstrated the neuroprotective effects of flavonoids derived from baical skullcap (Cho & Lee 2004, Heo et al 2004, Piao et al 2004, Shang et al 2006, Son et al 2004).
Cerebral ischaemia can cause a significant elevation in the concentrations of amino acid neurotransmitters in the cerebral cortex. Baical in administration can attenuate the elevations of glutamic acid and aspartic acid induced by cerebral ischaemia. This research demonstrates that baicalin may act as a neuroprotectant during cerebral ischaemia. Wogonin has been shown to exert a neuroprotective effect by inhibiting microglial activation, which is a critical component of pathogenic inflammatory responses in neurodegenerative diseases. Wogonin inhibited inflammatory activation of cultured brain microglia by diminishing lipopolysaccharide-induced TNF-alpha, IL-1 -beta and NO production. Wogonin inhibited NO production by suppressing iNOS induction and NF-kappa-B activation in microglia. The neuroprotective effect of wogonin has also been shown in vivo using two experimental brain injury models (Lee et al 2003).
A recent in vivo study in rats induced with permanent global ischaemia demonstrated that daily oral doses of baical skullcap flavonoids (35 mg/kg) for 19-20 days statistically increased learning and memory ability and attenuated neural injury (Shang et al 2005).
Baical skullcap is used in TCM for the treatment of stroke. Methanol extracts from the dried roots (0.1-10 mg/kg IP) significantly protected neurons against 10 min transient forebrain ischaemia. The extract inhibited microglial TNF-alpha and NO production, and protected cells from hydrogen peroxide-induced toxicity in vitro (Kim et al 2001).
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