Abstract
Delayed wound healing is one of the complications of diabetes mellitus, exhibited by profound inflammation and decreased granulation tissues. The current study was carried out to evaluate wound healing in both normal and diabetic rats. In addition, it evaluated the potential protective effect of transforming growth factor β1 (TGF β1), that has the broadest spectrum of actions, affecting all cell types that are involved in all stages of wound healing to accelerate wound healing in normal & diabetic rats. : The present study was performed on 40 male albino rats. Each 10 rats were designed as a group. Group I saved as control. They received incisional wound in their tongues 1 cm length and 1/2 cm depth. Group II received 500 ng/kg of TGF β1 5 minutes before wounding. Group III diabetes was induced then rats were treated as second group. At the 14(th) day post wounding, sections of tongues were taken for hematoxylin and eosin and Masson's trichome staining to examine the histological changes. The intracellular actions of TGF β1 were studied by TEM. A higher cell proliferation rate and a denser and more organized new extracellular matrix and complete wound closure was detected at the 14(th) days in the TGF β1 treated wound in comparison with the 14(th) days for the untreated, control groups. There were delayed wound healing in diabetic rats, decreased re-epithelialization, granulation tissue thickness, matrix density, number of infiltrated cells, and number of capillaries. In TGF β1 treated diabetic rats, showed significant healing improvement was obvious as compared with diabetic rats. A single intravenous injection of TGF β1 was sufficient to enhance wound healing in rat's tongue. This approach represents a new strategy that may be applied to the treatment of incisional wounds in human diabetic patients.
Highlights
Wound healing process can be defined as complex cascade that relies on several mechanisms for tissue repair that optimally leads to restoration of tissue integrity and function including coagulation, inflammation, ground substance and matrix synthesis, angiogenesis, wound contraction and remodeling. [1]
The aim of the present study is to examine the effect of transforming growth factor-beta1 on tongue wound healing in normal and alloxan-induced diabetic rats using light and transmission electron microscopes
Wounds in highrisk settings as diabetes mellitus would benefit from enhancing early wound healing
Summary
Wound healing process can be defined as complex cascade that relies on several mechanisms for tissue repair that optimally leads to restoration of tissue integrity and function including coagulation, inflammation, ground substance and matrix synthesis, angiogenesis, wound contraction and remodeling. [1]. [6] These growth factors induced proliferation of keratinocytes and fibroblasts, led to new formation of capillaries in the granulation tissue and modulated extracellular matrix deposition and reconstitution of the injured area They claimed that topical application of growth factors was successful to accelerate healing of full thickness wound in normal mice and normalize a delayed healing response of diabetic rats. [9] In addition, TGF-beta acts simultaneously as cellular stimulator to increase synthesis of most matrix protein by several folds, a cellular suppressor to decrease the production of inhibitors of certain collagen protease and modulator of integrin expression in a manner that increases cellular adhesion to the matrix These effect on EMC reflects the diverse biologic properties of TGFbeta and may be part of a negative feedback loop that normally regulates its own expression. The aim of the present study is to examine the effect of transforming growth factor-beta on tongue wound healing in normal and alloxan-induced diabetic rats using light and transmission electron microscopes
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