A study on evaluation of apoptosis and expression of bcl-2-related marker in wound healing of streptozotocin-induced diabetic rats.

ISRN Dermatology Pub Date : 2013-10-07 eCollection Date: 2013-01-01 DOI:10.1155/2013/739054
Surya Bhan, Rahul Mitra, A K Arya, H P Pandey, K Tripathi
{"title":"A study on evaluation of apoptosis and expression of bcl-2-related marker in wound healing of streptozotocin-induced diabetic rats.","authors":"Surya Bhan,&nbsp;Rahul Mitra,&nbsp;A K Arya,&nbsp;H P Pandey,&nbsp;K Tripathi","doi":"10.1155/2013/739054","DOIUrl":null,"url":null,"abstract":"<p><p>Uncontrolled blood sugar is a major cause of vascular complications and delayed wound healing in diabetes mellitus. During wound healing process, normally, apoptosis is responsible for events such as removal of inflammatory cells and evolution of granulation tissue into scar which occur during the late phase of wound healing. Early apoptosis can lead to abnormal wound healing by removing granulation tissue including fibroblast, endothelial cell, and small vessels. To determine the role of apoptosis in association with hyperglycemia in diabetic wound healing, apoptosis-related intracellular marker such as expression of Bcl-2 protein by immunohistochemistry and normal histology has been studied. Histological findings show higher level of apoptosis and diminished granulation tissue formation in diabetic rats wounds along with minimal expression of Bcl-2 in diabetic rats wounds when compared with nondiabetic rats wounds. It can be concluded from this study that elevated blood sugar level may be associated with increased apoptosis and the least expression of Bcl-2 protein which might cause deregulation of the wound healing processes in streptozotocin-induced diabetic rats. </p>","PeriodicalId":14682,"journal":{"name":"ISRN Dermatology","volume":"2013 ","pages":"739054"},"PeriodicalIF":0.0000,"publicationDate":"2013-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/739054","citationCount":"28","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"ISRN Dermatology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1155/2013/739054","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2013/1/1 0:00:00","PubModel":"eCollection","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 28

Abstract

Uncontrolled blood sugar is a major cause of vascular complications and delayed wound healing in diabetes mellitus. During wound healing process, normally, apoptosis is responsible for events such as removal of inflammatory cells and evolution of granulation tissue into scar which occur during the late phase of wound healing. Early apoptosis can lead to abnormal wound healing by removing granulation tissue including fibroblast, endothelial cell, and small vessels. To determine the role of apoptosis in association with hyperglycemia in diabetic wound healing, apoptosis-related intracellular marker such as expression of Bcl-2 protein by immunohistochemistry and normal histology has been studied. Histological findings show higher level of apoptosis and diminished granulation tissue formation in diabetic rats wounds along with minimal expression of Bcl-2 in diabetic rats wounds when compared with nondiabetic rats wounds. It can be concluded from this study that elevated blood sugar level may be associated with increased apoptosis and the least expression of Bcl-2 protein which might cause deregulation of the wound healing processes in streptozotocin-induced diabetic rats.

Abstract Image

Abstract Image

Abstract Image

链脲佐菌素诱导的糖尿病大鼠创面愈合过程中凋亡及bcl-2相关标志物表达的研究。
血糖失控是糖尿病血管并发症和伤口延迟愈合的主要原因。在伤口愈合过程中,通常情况下,细胞凋亡负责炎症细胞的清除和肉芽组织向瘢痕的演变等事件,这些事件发生在伤口愈合的后期。早期细胞凋亡可通过去除肉芽组织(包括成纤维细胞、内皮细胞和小血管)导致伤口异常愈合。为了确定细胞凋亡与高血糖在糖尿病创面愈合中的作用,我们通过免疫组织化学和正常组织学研究了细胞凋亡相关的细胞内标志物,如Bcl-2蛋白的表达。组织学结果显示,与非糖尿病大鼠相比,糖尿病大鼠创面细胞凋亡水平升高,肉芽组织形成减少,Bcl-2表达减少。本研究提示,血糖升高可能与链脲佐菌素诱导的糖尿病大鼠创面愈合过程中凋亡增加和Bcl-2蛋白表达减少有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信