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Mechanistic study of endogenous skin lesions in diabetic rats
Xiang-fang Chen1, Wei-dong Lin, Shu-liang Lu
1Department of Endocrinology, Chang Zheng Hospital, Second Military Medical University, Shanghai, China.
Abstract:
Pathological and physiological changes in dermal tissue in a rat model of diabetes mellitus (DM) were investigated. Sixteen male 8-week-old Sprague-Dawley rats were randomized into two groups of eight, the DM group (Group DM) and the normal control group (Group (NC) normal control). Group DM rats were injected with streptozotocin (STZ) intraperitoneally at a dose of 65 mg/kg body weight. Group NC rats were injected with the same volume of citric acid buffer. All rats were sacrificed 12 weeks later. The impact of exposure to (AGE) advanced glycation end products-modified human serum albumin (AGE-HSA) on epidermal cells and ECV304 cells was evaluated in cell culture experiments. The diabetic rats exhibited changes in skin tissue, including a decrease in thickness, disappearance of the multilayer epithelium structure, degeneration of collagen fibres and an increase in the infiltration of inflammatory cells, in addition to a significant increase in skin glucose and AGEs. Moreover, diabetic rats had increased plasma glycosylated protein (GSP) and malondialdehyde (MDA) and decreased plasma glutathione (GSH). The percentage of epidermal cells in S phase was similar between the two group rats; however, there was a marked decrease in the G2/M phase in Group DM. Additionally, exposure of ECV304 cells to AGE-HSA led to a time-dependent and dose-dependent increase in apoptosis. Therefore, the high glucose in the skin tissue, coupled with the accumulation of toxic substances such as AGEs, promote the dysfunction of dermal cells and/or the matrix. This may be a significant mechanism of diabetes-induced early-stage endogenous skin damage.
Insights
Diabetes mellitus causes skin damage by increasing skin glucose and advanced glycation end products (AGEs), leading to dermal cell dysfunction. This study reveals a key mechanism in diabetes-induced skin injury.
Area of Science:
- Dermatology
- Endocrinology
- Pathology
Background:
- Diabetes mellitus (DM) is associated with various complications, including skin damage.
- Understanding the early mechanisms of diabetes-induced skin alterations is crucial for effective management.
Purpose of the Study:
- To investigate the pathological and physiological changes in dermal tissue in a rat model of diabetes mellitus.
- To evaluate the impact of advanced glycation end products (AGEs) on skin cells.
Main Methods:
- A rat model of diabetes mellitus was established using streptozotocin (STZ).
- Skin tissue and plasma parameters were analyzed 12 weeks post-induction.
- In vitro experiments assessed the effect of AGE-modified human serum albumin (AGE-HSA) on epidermal and ECV304 cells.
Main Results:
- Diabetic rats showed decreased skin thickness, epithelial structure loss, collagen degeneration, and increased inflammatory cell infiltration.
- Elevated skin glucose, AGEs, plasma glycosylated protein (GSP), and malondialdehyde (MDA) were observed, with decreased plasma glutathione (GSH).
- Exposure to AGE-HSA induced apoptosis in ECV304 cells in a time- and dose-dependent manner.
Conclusions:
- High skin glucose and AGE accumulation contribute to dermal cell and matrix dysfunction in diabetes.
- These factors represent a significant mechanism underlying early-stage, endogenous skin damage in diabetes mellitus.
