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Anthralin-induced oxidative stress m...

Lange, Robert William.

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Anthralin-induced oxidative stress modulates inflammatory cytokine gene expression in human keratinocytes and the BALB/c mouse ear.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Anthralin-induced oxidative stress modulates inflammatory cytokine gene expression in human keratinocytes and the BALB/c mouse ear./
作者:	Lange, Robert William.
面頁冊數:	86 p.
附註:	Source: Dissertation Abstracts International, Volume: 58-03, Section: B, page: 1246.
Contained By:	Dissertation Abstracts International58-03B.
標題:	Health Sciences, Toxicology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9726076
ISBN:	0591349892

Anthralin-induced oxidative stress modulates inflammatory cytokine gene expression in human keratinocytes and the BALB/c mouse ear.
Lange, Robert William.

Anthralin-induced oxidative stress modulates inflammatory cytokine gene expression in human keratinocytes and the BALB/c mouse ear. - 86 p.

Source: Dissertation Abstracts International, Volume: 58-03, Section: B, page: 1246.

Thesis (Ph.D.)--North Carolina State University, 1997.

The purpose of the research was three-fold: (1) to examine anthralin-induced changes in inflammatory cytokine gene expression in primary human keratinocyte cultures and the mouse skin, (2) determine the role of anthralin-induced, reactive oxygen species in the observed cytokine changes, (3) determine whether anthralin directly stimulates chemokine gene expression in human keratinocytes. Keratinocytes respond to stimuli by producing cytokines, growth factors, adhesion molecules, and chemotactic factors (acting in a network) responsible, in part, for initiation of cutaneous inflammation. Anthralin induces IL-6, human IL-8 or murine MIP-2, GM-CSF, and TNF

ISBN: 0591349892Subjects--Topical Terms:

1017752
Health Sciences, Toxicology.

Anthralin-induced oxidative stress modulates inflammatory cytokine gene expression in human keratinocytes and the BALB/c mouse ear.
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245 1 0 $a Anthralin-induced oxidative stress modulates inflammatory cytokine gene expression in human keratinocytes and the BALB/c mouse ear.
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500 $a Source: Dissertation Abstracts International, Volume: 58-03, Section: B, page: 1246.
500 $a Directors: Michael I. Luster; Robert C. Smart.
502 $a Thesis (Ph.D.)--North Carolina State University, 1997.
520 $a The purpose of the research was three-fold: (1) to examine anthralin-induced changes in inflammatory cytokine gene expression in primary human keratinocyte cultures and the mouse skin, (2) determine the role of anthralin-induced, reactive oxygen species in the observed cytokine changes, (3) determine whether anthralin directly stimulates chemokine gene expression in human keratinocytes. Keratinocytes respond to stimuli by producing cytokines, growth factors, adhesion molecules, and chemotactic factors (acting in a network) responsible, in part, for initiation of cutaneous inflammation. Anthralin induces IL-6, human IL-8 or murine MIP-2, GM-CSF, and TNF $\ alpha $ mRNAs in primary human keratinocyte cultures and the mouse skin and IL-8 and TNF secretion in primary human keratinocyte cultures. Pretreatment of keratinocytes or BALB/c mice with antioxidants selectively inhibited anthralin-induced cytokines. Of particular note was the inhibition of the chemokine human IL-8 and murine MIP-2 by vitamin E and GM-CSF and TNF $\ alpha $ by superoxide dismutase, as well as mouse ear swelling and inflammatory cell infiltration. The expression of the chemokine, IL-8, was independent of the paracrine activity of TNF $\ alpha $ but was induced by reactive oxygen species. The activity of a transfected CAT-linked IL-8 promoter containing potential binding sites for NF-IL-6, NF- $\ kappa
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650 4 $a Health Sciences, Immunology. $3 1017716
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