Abstract
Background Burns are wounds caused by exposure to an agent from thermal, electric, radioactive or chemistry origin which presents attenuated inflammatory response, becoming even more compromised when associated to diabetes mellitus. Despite the fact from experimental evidences demonstrating tissue healing and reconstruction acceleration due to topical insulin used in diabetic and control rats with incised wounds and burn wounds in diabetic rats, however there is no information regarding molecular and cellular mechanism of topical insulin upon burn wounds.
Highlights
Burns are wounds caused by exposure to an agent from thermal, electric, radioactive or chemistry origin which presents attenuated inflammatory response, becoming even more compromised when associated to diabetes mellitus
Treatment with topical insulin induced early enhancement of macrophages infiltration in the wound surroundings detected by MCP-1 and F4/80 antibodies at day 7 and increased in KGF expression (p
At 14th day after burn induction accompanied by enhanced angiogenesis, detected with VEGF and TGF-b1 antibodies; increased expression of alpha smooth muscle actin, present in mature blood vessels; increased cell proliferation, detected with Ki67 antibody on groups treated with topical insulin (DI), when compared to DP
Summary
Burns are wounds caused by exposure to an agent from thermal, electric, radioactive or chemistry origin which presents attenuated inflammatory response, becoming even more compromised when associated to diabetes mellitus. Despite the fact from experimental evidences demonstrating tissue healing and reconstruction acceleration due to topical insulin used in diabetic and control rats with incised wounds and burn wounds in diabetic rats, there is no information regarding molecular and cellular mechanism of topical insulin upon burn wounds
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