Bee Gomogenat Accelerates Diabetic Wound Healing by Regulating Gap Junction Proteins
Abstract: This article presents a study investigating the effects of bee gomogenat (BG) on the healing process of diabetic wounds in a streptozotocin-induced type-1 diabetes mouse model. The research focuses on the impact of BG on various aspects of wound healing, including collagen deposition, angiogenesis, inflammation markers, and expression levels of connexin-pannexin gap junction proteins. The results demonstrate that BG treatment significantly enhances the healing process, providing potential therapeutic benefits for diabetic-related wounds.
Introduction: The delayed healing of wounds is a common complication associated with diabetes mellitus, leading to increased mortality. This study explores the potential therapeutic effects of bee gomogenat (BG) on diabetic wound closure by examining its impact on collagen deposition, angiogenesis, and inflammation markers. The investigation also delves into the regulation of connexin-pannexin gap junction proteins, essential for intercellular communication during skin homeostasis and wound healing.
Materials and Methods: The study utilized a streptozotocin-induced type-1 diabetes mouse model, dividing the rodents into three groups: non-diabetic controls, diabetic rodents, and BG-treated diabetic rodents. Various assessments, including biochemical evaluations, histological examinations, and immunohistochemistry studies, were conducted to analyze the effects of BG on wound healing parameters.
Results: BG treatment demonstrated a significant improvement in body weight and blood glucose concentrations in diabetic mice. Histopathological analysis revealed that BG-treated diabetic rodents exhibited enhanced wound closure, reduced inflammation, increased granulation tissue, and improved re-epithelization compared to untreated diabetic mice. Furthermore, BG treatment led to increased collagen deposition, down-regulation of pro-inflammatory markers (MCP-1 and HSP-70), and restored expression levels of connexin-pannexin gap junction proteins (Cx43 and Panx3).
Discussion: The study emphasizes the association between diabetes-induced complications and impaired wound healing, attributing the delay to factors such as reduced collagen production, abnormal angiogenesis, and inflammation. BG treatment addresses these issues, promoting active angiogenesis, reducing inflammation, and restoring the expression of crucial gap junction proteins. The results suggest BG as a potential novel strategy for improving diabetic wound closure.
Conclusion: This research provides novel insights into the therapeutic effects of bee gomogenat on diabetic wound healing. BG treatment demonstrates a significant enhancement in various aspects of the healing process, making it a promising candidate for addressing the serious consequences of impaired wound healing in diabetes. Further studies are warranted to explore the specific mechanisms through which BG exerts its beneficial effects.
Acknowledgments: The study was conducted with ethical approval from the Research Ethical Committee of the Faculty of Science, Assiut University, Egypt. The authors acknowledge the support from Etman colonies in Tanta, Egypt, for providing bee gomogenat.
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