금은화의 NF-κB 활성 억제를 통한 iNOS 조절이 NC/Nga 생쥐의 아토피 피부염에 미치는 영향
Lonicera Japonica Inhibits Atopy Dermatitis in NC/Nga Mouse through Regulation of iNOS by NF-κB Suppression
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초록
Inducible nitric oxide synthase (iNOS) are important inflammation enzyme and severe up-nitric oxide (NO) production by this enzyme has been intricate with pathogenesis of atopy dermatitis. The present study was designed in order to determine whether Lonicera japonica could inhibit atopy dermatitis through modulation of iNOS by NF-κB suppression. We found that IKK mRNA and iNOS mRNA expression in RAW 264.7 macrophages stimulated with lipopolysaccharide dose-dependantly decreased by Lonicera japonica (0.4 - 1.0 ㎎/㎖) and NO production decreased. The distribution of NF-κB p65 and iNOS positive reacted cell in NC/Nga mice with atopy dermatitis were decreased by Lonicera japonica (45 ㎎/㎏/day) and apoptosis were increased. These data likely indicate that Lonicera japonica may act as inflammatory regulator for atopy dermatitis through iNOS modulation by NF-κB suppression and may be possible to develop useful agent for chemoprevention of NO intricate inflammatory diseases.
Abstract
Inducible nitric oxide synthase (iNOS) are important inflammation enzyme and severe up-nitric oxide (NO) production by this enzyme has been intricate with pathogenesis of atopy dermatitis. The present study was designed in order to determine whether Lonicera japonica could inhibit atopy dermatitis through modulation of iNOS by NF-κB suppression. We found that IKK mRNA and iNOS mRNA expression in RAW 264.7 macrophages stimulated with lipopolysaccharide dose-dependantly decreased by Lonicera japonica (0.4 - 1.0 ㎎/㎖) and NO production decreased. The distribution of NF-κB p65 and iNOS positive reacted cell in NC/Nga mice with atopy dermatitis were decreased by Lonicera japonica (45 ㎎/㎏/day) and apoptosis were increased. These data likely indicate that Lonicera japonica may act as inflammatory regulator for atopy dermatitis through iNOS modulation by NF-κB suppression and may be possible to develop useful agent for chemoprevention of NO intricate inflammatory diseases.
참고문헌 (40)
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