Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0849640 (skin damage)
 1,516 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Local skin trauma induces inflammatory responses resulting in local tissue and distant organ injury. EGF, a polypeptide hormone, mainly produced in saliva, is one of the major accelerators in wound healing. Wistar albino rats of both sexes received either bovine serum albumin or EGF (10 microg/kg) subcutaneously before a circular (18 mm diameter) partial thickness burn was induced. Afterwards, some rats were placed in separate cages to prevent licking, while the others were caged together to allow wound-licking. Treatments were continued for 5 more days and on the 5th day animals were decapitated. Histopathological analysis of skin damage and dermal myeloperoxidase (MPO) activity, as an index for neutrophil activity, were evaluated. Oxidant injury to the liver and intestines was determined by measuring glutathione (GSH) and malondialdehyde (MDA) levels, as well as MPO activity. The results demonstrate that healing of the burn wound on the skin is accelerated by both wound-licking and EGF administration, which also attenuated tissue neutrophil accumulation, suggesting the role of neutrophils as the source of mediators involved in delayed epithelial regeneration. Moreover, local dermal burn results in oxidant injury to the liver, concomitant with significant elevations in hepatic and intestinal GSH levels. Exogenous administration of EGF at physiological doses had no effect on inflammatory responses of the distant organs, while allowing the rats to lick the wound reduced the oxidant injury to the liver. Since saliva or EGF enhances skin wound healing, topical use of EGF-rich artificial saliva merits consideration for its use in burn patients.
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PMID:The healing-promoting effect of saliva on skin burn is mediated by epidermal growth factor (EGF): role of the neutrophils. 1530 17

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.
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PMID:Mechanistic study of endogenous skin lesions in diabetic rats. 2070 29