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。

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
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引用次数: 28

摘要

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。

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

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.

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