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The role of nutrition during the ear...
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Lim, Yunsook.
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The role of nutrition during the early inflammatory stage of cutaneous wound healing.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
The role of nutrition during the early inflammatory stage of cutaneous wound healing./
作者:
Lim, Yunsook.
面頁冊數:
140 p.
附註:
Source: Dissertation Abstracts International, Volume: 65-01, Section: B, page: 0164.
Contained By:
Dissertation Abstracts International65-01B.
標題:
Health Sciences, Nutrition. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3119477
ISBN:
0496668684
The role of nutrition during the early inflammatory stage of cutaneous wound healing.
Lim, Yunsook.
The role of nutrition during the early inflammatory stage of cutaneous wound healing.
- 140 p.
Source: Dissertation Abstracts International, Volume: 65-01, Section: B, page: 0164.
Thesis (Ph.D.)--The Ohio State University, 2003.
Reactive oxygen species (ROS) and proinflammatory cytokines produced by immune cells during inflammation activate NFkappaB, a redox sensitive transcription factor that induces expression of immunoregulatory genes such as chemokines and cytokines during the inflammatory stage. NFkappaB activation and proinflammatory cytokine production play key roles in regulating wound healing. Notably, protein energy malnutrition (PEM) and zinc deficiency are well-known health problems associated with delayed wound healing. N-acetyl cysteine (NAC) supplementation in PEM may help wound healing by enhancing immune response and antioxidant defense. Zinc supplementation may also increase immune function and antioxidant defense. Therefore, this dissertation was focused upon the role of nutrition and ROS in wound closure and the effect of nutritional supplementation on immune response and antioxidant defense at cellular and molecular levels during the early inflammatory stage of cutaneous wound healing.
ISBN: 0496668684Subjects--Topical Terms:
1017801
Health Sciences, Nutrition.
The role of nutrition during the early inflammatory stage of cutaneous wound healing.
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Source: Dissertation Abstracts International, Volume: 65-01, Section: B, page: 0164.
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Thesis (Ph.D.)--The Ohio State University, 2003.
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Reactive oxygen species (ROS) and proinflammatory cytokines produced by immune cells during inflammation activate NFkappaB, a redox sensitive transcription factor that induces expression of immunoregulatory genes such as chemokines and cytokines during the inflammatory stage. NFkappaB activation and proinflammatory cytokine production play key roles in regulating wound healing. Notably, protein energy malnutrition (PEM) and zinc deficiency are well-known health problems associated with delayed wound healing. N-acetyl cysteine (NAC) supplementation in PEM may help wound healing by enhancing immune response and antioxidant defense. Zinc supplementation may also increase immune function and antioxidant defense. Therefore, this dissertation was focused upon the role of nutrition and ROS in wound closure and the effect of nutritional supplementation on immune response and antioxidant defense at cellular and molecular levels during the early inflammatory stage of cutaneous wound healing.
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We have hypothesized that malnutrition delays cutaneous wound closure due to decreased immune response and antioxidant defense. Furthermore, we propose that nutritional supplementation will restore immune function and antioxidant defense in the inflammatory stage during cutaneous wound healing. To test these hypotheses, we have: (i) investigated the effects of PEM and the role of ROS using CuZnSOD transgenic mice to determine if malnutrition or ROS affect cutaneous wound healing; (ii) examined the role of dietary supplementation of NAC on wound closure and gene expression of pro-inflammatory cytokines (IL-1beta and TNF-alpha) and IKB (indirect measurement of NFkappaB activation) during the early inflammatory stage in PEM mice; and (iii) investigated the role of dietary zinc on wound closure and gene expression of IL-1beta, TNF-alpha and IkappaB.
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The results of these experiments demonstrated that PEM impaired wound healing, possibly due to delayed neutrophil infiltration and decreased gene expression of IkappaB, IL-1beta and TNF-alpha. However, NAC supplementation restored neutrophil response and normalized gene expression of IkappaB, IL-1beta and TNF-alpha in the early inflammatory stage of cutaneous wound healing. In addition, we found that zinc deficiency delayed wound closure. Notably, we also found that zinc supplementation at 500 ppm accelerated neutrophil infiltration, increased expression of IkappaB and enhanced wound closure. However, mega dose zinc supplementation at 1000 ppm (20 times higher than that of a control diet) delayed neutrophil infiltration, decreased IkappaB levels and delayed normal wound closure. (Abstract shortened by UMI.)
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