The anti-inflammatory activity of baical skullcap has been well documented by in vitro and in vivo studies. The main constituents responsible are baicalein and wogonin (Chang et al 2001, Chi et al 2001, Chung et al 1995, Krakauer et al 2001, Li et al 2000, Park et al 2001, Wakabayashi 1999).
In a study using mice, baicalein 50 mg/kg has been shown to ameliorate the inflammatory symptoms of induced colitis, including body weight loss, blood haemoglobin content, rectal bleeding and other histological and biochemical parameters (Hong et al 2002). Pretreatment with wogonin also significantly reduced ethanol-induced gastric damage in vivo (Park et al 2004) and reduced immunoglobulin E, IL-4, IL-5 and IL-10 secretion in a colitis-induced mouse model (Lim 2004). The methanolic extract of the baical skullcap root and its flavonoids wogonin, baicalein and baicalin have been shown to inhibit lipopolysaccharide-induced inflammation of the gingivae (gums) in vivo. The three flavonoids exerted an anti-inflammatory effect similar to prednisolone. In addition, the flavonoids exerted a moderate inhibition (33-36%) of collagenolytic activity, comparable to the 40% inhibition by tetracycline. Meanwhile, the cellular activity of fibroblasts was augmented remarkably (40%) by baicalein and slightly by baicalin and wogonin. Consistent with the cellular activation, the flavonoids enhanced the synthesis of both collagen and total protein in fibroblasts in vitro (Chung et al 1995).
The anti-inflammatory mechanisms are varied and summarised below. Chemokine binding It has been proposed that the anti-inflammatory activity is partly caused by limiting the biological function of chemokines.
Excessive release of pro-inflammatory cytokines mediates the toxic effect of superantigenic staphylococcal exotoxins. In vitro data suggest that baicalin may be therapeutically useful for mitigating the pathogenic effects of staphylococcal exotoxins by inhibiting the signalling pathways activated by superantigens (Krakauer et al 2001).
Baicalin inhibited the binding of a number of chemokines to human leukocytes or cells expressing specific chemokine receptors, with an associated reduced capacity of the chemokines to induce cell migration. Based on these results, it is possible that the anti-inflammatory mechanism of baicalin is to bind a variety of chemokines and limit their biological function (Bao et al 2000, Li et al 2000).
Four major flavonoids from baical have been shown in vitro to suppress eotaxin. Eotaxin is an eosinophil-specific chemokine associated with the recruitment of eosinophils to sites of allergic inflammation. Eotaxin is produced by IL-4 plus TNF- Baical skullcap 58
alpha-stimulated human fibroblasts. This may explain why it has been used
traditionally in the treatment of bronchial asthma (Nakajima et al 2001). Various flavonoids, including wogonin and baicalein, have been shown to inhibit chemically induced histamine release from rat mast cells in vitro (Kubo et al 1984). COX-2 inhibition Wogonin is a direct COX-2 inhibitor. Wogonin inhibits both inducible nitric oxide synthase and cyclo-oxygenase 2 induction (Chen et al 2001, Chi et al 2001, Wakabayashi & Yasui 2000). Wogonin has been shown to inhibit inducible PGE2 production in macrophages by inhibiting COX-2 (Wakabayashi &Yasui 2000).
Wogonin may be beneficial for COX-2-related skin disorders. When applied topically to the dorsal skin of mice, it inhibited COX-2 expression and PGE2 production (Byoung et al 2001, Chi et al 2003, Park et al 2001). Lipoxygenase inhibition The inhibition of the 5-lipoxygenase pathway of arachidonic acid metabolism may be one of the mechanisms of baicalein's antiinflammatory activity according to an in vivo study (Butenko et al 1993). Nitric oxide synthase inhibition Baicalein and wogonin attenuate lipopolysaccharide-stimulated nitric oxide synthase induction in macrophages, which helps to explain the anti-inflammatory action of these flavonoid compounds (Wakabayashi 1999).
Antioxidant activity The anti-inflammatory activity of baicalein may be associated with inhibition of leukocyte adhesion by the scavenging of reactive oxygen intermediates (Shen et al 2003).
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