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Planta Med. 2013 Mar;79(3-4):199-206. doi: 10.1055/s-0032-1328197. Epub 2013 Feb 1.

Effects of baicalin on airway remodeling in asthmatic mice.

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  • 1Department of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai, China.


Airway remodeling is an important characteristic of asthma, linking inflammation with airway hyperresponsiveness. Baicalin, a major active component, was isolated from Radix Scutellariae. Many studies show that baicalin has anti-inflammatory, anti-bacterial, and anti-allergic effects. Here we investigate the influence of baicalin on asthmatic airway remodeling and the mechanism underlining the anti-remodeling effect in vivo.Asthmatic airway remodeling mice model was established by ovalbumin exposure. Seventy female BALB/c mice were randomly assigned to seven experimental groups: blank, ovalbumin, hexadecadrol, control, and baicalin (25 mg/kg, 50 mg/kg, 100 mg/kg) groups. Pulmonary function was measured using a whole-body plethysmograph in conscious and unrestrained mice. The lung pathology was observed and measured. The production of cytokines in bronchoalveolar lavage fluid and serum was measured using enzyme-labeled immunosorbent assay kits, and the expression levels of transforming growth factor-β1 and vascular endothelial growth factor were detected by immunohistochemistry. The protein expression levels of transforming growth factor-β1, vascular endothelial growth factor, extracellular signal-regulated kinase, and p21ras were measured using Western blot. The results show that ovalbumin exposure significantly increased the expression of interleukin-13 in BALF and serum, and transforming growth factor-β1, vascular endothelial growth factor, extracellular signal-regulated kinase and p21ras expressions in the lungs. Baicalin attenuated the effects of ovalbumin significantly.It can be concluded that baicalin has significant anti-remodeling effect on ovalbumin-induced asthmatic airway remodeling mice model by decreasing expression of transforming growth factor-β1, interleukin-13, and vascular endothelial growth factor and inhibiting the activation of the extracellular signal-regulated kinase pathway.

Georg Thieme Verlag KG Stuttgart · New York.

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