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Up-regulation of Hsp72 and keratin16 mediates wound healing in streptozotocin diabetic rats

BACKGROUND: Impaired wound healing is a complication of diabetes and a serious problem in clinical practice. We previously found that whey protein (WP) was able to regulate wound healing normally in streptozotocin (STZ)-diabetic models. This subsequent study was designed to assess the effect of WP o...

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Autores principales: Ahmed, Rasha R., Mahmoud, Ayman, Ahmed, Osama M., Metwalli, Ali, Ebaid, Hossam
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4591711/
https://www.ncbi.nlm.nih.gov/pubmed/26428860
http://dx.doi.org/10.1186/s40659-015-0044-5
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author Ahmed, Rasha R.
Mahmoud, Ayman
Ahmed, Osama M.
Metwalli, Ali
Ebaid, Hossam
author_facet Ahmed, Rasha R.
Mahmoud, Ayman
Ahmed, Osama M.
Metwalli, Ali
Ebaid, Hossam
author_sort Ahmed, Rasha R.
collection PubMed
description BACKGROUND: Impaired wound healing is a complication of diabetes and a serious problem in clinical practice. We previously found that whey protein (WP) was able to regulate wound healing normally in streptozotocin (STZ)-diabetic models. This subsequent study was designed to assess the effect of WP on heat shock protein-72 (Hsp72) and keratin16 (Krt16) expression during wound healing in diabetic rats. METHODS: WP at a dosage of 100 mg/kg of body weight was orally administered daily to wounded normal and STZ-diabetic rats for 8 days. RESULTS: At day 4, the WP-treated diabetic wound was significantly reduced compared to that in the corresponding control. Diabetic wounded rats developed severe inflammatory infiltration and moderate capillary dilatation and regeneration. Treated rats had mild necrotic formation, moderate infiltration, moderate to severe capillary dilatation and regeneration, in addition to moderate epidermal formation. Hsp72 and Krt16 densities showed low and dense activity in diabetic wounded and diabetic wounded treated groups, respectively. At day 8, WP-treatment of diabetic wounded animals revealed great amelioration with complete recovery and closure of the wound. Reactivity of Hsp72 and Krt16 was reversed, showing dense and low, or medium and low, activity in the diabetic wounded and diabetic wounded treated groups, respectively. Hsp72 expression in the pancreas was found to show dense reactivity with WP-treated diabetic wound rats. CONCLUSION: This data provides evidence for the potential impact of WP in the up-regulation of Hsp72 and Krt16 in T1D, resulting in an improved wound healing process in diabetic models.
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spelling pubmed-45917112015-10-03 Up-regulation of Hsp72 and keratin16 mediates wound healing in streptozotocin diabetic rats Ahmed, Rasha R. Mahmoud, Ayman Ahmed, Osama M. Metwalli, Ali Ebaid, Hossam Biol Res Research Article BACKGROUND: Impaired wound healing is a complication of diabetes and a serious problem in clinical practice. We previously found that whey protein (WP) was able to regulate wound healing normally in streptozotocin (STZ)-diabetic models. This subsequent study was designed to assess the effect of WP on heat shock protein-72 (Hsp72) and keratin16 (Krt16) expression during wound healing in diabetic rats. METHODS: WP at a dosage of 100 mg/kg of body weight was orally administered daily to wounded normal and STZ-diabetic rats for 8 days. RESULTS: At day 4, the WP-treated diabetic wound was significantly reduced compared to that in the corresponding control. Diabetic wounded rats developed severe inflammatory infiltration and moderate capillary dilatation and regeneration. Treated rats had mild necrotic formation, moderate infiltration, moderate to severe capillary dilatation and regeneration, in addition to moderate epidermal formation. Hsp72 and Krt16 densities showed low and dense activity in diabetic wounded and diabetic wounded treated groups, respectively. At day 8, WP-treatment of diabetic wounded animals revealed great amelioration with complete recovery and closure of the wound. Reactivity of Hsp72 and Krt16 was reversed, showing dense and low, or medium and low, activity in the diabetic wounded and diabetic wounded treated groups, respectively. Hsp72 expression in the pancreas was found to show dense reactivity with WP-treated diabetic wound rats. CONCLUSION: This data provides evidence for the potential impact of WP in the up-regulation of Hsp72 and Krt16 in T1D, resulting in an improved wound healing process in diabetic models. BioMed Central 2015-10-01 /pmc/articles/PMC4591711/ /pubmed/26428860 http://dx.doi.org/10.1186/s40659-015-0044-5 Text en © Ahmed et al. 2015 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Ahmed, Rasha R.
Mahmoud, Ayman
Ahmed, Osama M.
Metwalli, Ali
Ebaid, Hossam
Up-regulation of Hsp72 and keratin16 mediates wound healing in streptozotocin diabetic rats
title Up-regulation of Hsp72 and keratin16 mediates wound healing in streptozotocin diabetic rats
title_full Up-regulation of Hsp72 and keratin16 mediates wound healing in streptozotocin diabetic rats
title_fullStr Up-regulation of Hsp72 and keratin16 mediates wound healing in streptozotocin diabetic rats
title_full_unstemmed Up-regulation of Hsp72 and keratin16 mediates wound healing in streptozotocin diabetic rats
title_short Up-regulation of Hsp72 and keratin16 mediates wound healing in streptozotocin diabetic rats
title_sort up-regulation of hsp72 and keratin16 mediates wound healing in streptozotocin diabetic rats
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4591711/
https://www.ncbi.nlm.nih.gov/pubmed/26428860
http://dx.doi.org/10.1186/s40659-015-0044-5
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