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. 1. Introduction Apoptosis is a physiological cell death process, possesses very distinct features, and is almost different from necrosis which is characterized by morphological changes, including DNA fragmentation, membrane alteration, and formation of apoptotic bodies. It is one of the physiological cell death processes, which governs developmental biology and cellular homeostasis in an organism. There is enormous kind of evidence that the sequence of cellular events that characterize healing of cutaneous wound and other tissue repair processes is tightly regulated and controlled by a distinct temporal pattern of cellular apoptosis [1]. The three classically defined phases of wound healing, that is, inflammation, tissue formation, and tissue remodeling involve the differential participation of resident cells and infiltrating leukocyte subtypes [2]. After the initial haemostatic event, early wound repair is characterized by the invasion of neutrophils, macrophages, and lymphocytes, which serves as source of inflammatory and growth-promoting cytokines [3]. The fibroblasts migrate, proliferate, and synthesize extracellular matrix components, participating in the formation of granulation tissue. Cellular infiltration and proliferation must be sufficient and pronounced for normal early progression of wound repair. It has been discussed that this rapid increase in cell proliferation is allowed
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