Table of Contents
ISRN Dermatology
Volume 2013, Article ID 739054, 6 pages
Research Article

A Study on Evaluation of Apoptosis and Expression of Bcl-2-Related Marker in Wound Healing of Streptozotocin-Induced Diabetic Rats

1Department of Biochemistry, School of Life Sciences, NEHU, Shillong 793022, India
2Department of Biochemistry, Institute of Medical Sciences, Banaras Hindu University, Varanasi 221005, India
3Department of Medicine, Institute of Medical Sciences, Banaras Hindu University, Varanasi 221005, India
4Department of Biochemistry, Faculty of Science, Banaras Hindu University, Varanasi 221005, India

Received 17 July 2013; Accepted 28 August 2013

Academic Editors: Y. Tuzun and W. Vanscheidt

Copyright © 2013 Surya Bhan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.