The Effects of Bangpungtongsungsan Extract to the Skin Damage on Mice Model after Atopic Dermatitis Elicitation

방풍통성산(防風通聖散)이 아토피 피부염을 유발한 동물모델의 피부 손상에 미치는 영향

  • 손정민 (동국대학교 한의과대학 한방안이비인후피부과학교실) ;
  • 홍승욱 (동국대학교 한의과대학 한방안이비인후피부과학교실)
  • Published : 2007.04.25

Abstract

Objectives : Atopic dermatitis has a close relationship with damage of skin barrier function. To investigate the effects of Bangpungtongsungsan(BT) extract to the skin damage on mice model after atopic dermatitis elicitation, this study was done through forcing injury to mice's skin. Methods : The BALB/c mice were distributed into three groups: control(CON) group, atopic dermatitis(AD)-elicited group, Bangpungtongsungsan(BT)-treated group. AD-elicited and BT-treated group were caused AD according to the method of Christophers E., Mrowietz and Minehiro. The BT extract was administered for 48 hours to BT-treated group. We observed changes of external dermal formation, eosinophils in vasculature, lipid formation in stratum corneum, distribution of ceramide, distribution of capillary, $I{\kappa}B$ kinase(IKK) and induce nitric oxide synthase(iNOS) mRNA expression. We used the statistical methods of student t-test(p<0.05). Results : After dispensing BT extract into the AD-elicited group, the number of eosinophil as an atopic index in mice noticeably decreased and dermal injury decreased. Also the decrease of hyperplasia, degranulated mast cells, angiogenesis and substance P were shown. The lipid lamellae, lipid protect formation, were repaired and the distribution of ceramide which inhibit protein kinase C(PKC) activation increased, and the PKC caused inhibition of nuclear $factor(NF)-{\kappa}B$ activation. As a result of inhibition of $NF-{\kappa}B$ activation, iNOS production were inhibited and apoptotic cell were increased. Moreover the decrease of IKK and iNOS mRNA expression in BT-treated RAW 264.7 cell were noted. Conclusion : BT mitigated skin damage on mice model after atopic dermatitis elicitation through recovering skin barrier function and inhibiting nuclear $factor(NF)-{\kappa}B$ activation.

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