Propranolol impairs the closure of pressure ulcers in mice

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• 作者：Thatiana L. Assis de Brito ; André ; a Monte-Alto-Costa ; Bruna Romana-Souza ; ^{romanabio@yahoo.com.br" class="auth_mail} ; ^{bruna.souza@uerj.br" class="auth_mail}
• 关键词：Propranolol hydrochloride (PubChem CID ; 62882) ; Ketamine (PubChem CID ; 3821) ; Xylazine (PubChem CID ; 5707) ; Formalin (PubChem CID ; 712) ; Diaminobenzidine (PubChem CID ; 7071) ; Hematoxylin (PubChem CID ; 442514) ; Sodium dodecylsulfate (PubChem CID ; 3423265) ; Polyacrylamide (PubChem CID ; 6579) ; Methanol (PubChem CID ; 887) ; Xylenol orange (PubChem CID ; 16220156) ; Sulfuric acid (PubChem CID ; 1118) ; Hydrochloric acid (PubChem CID ; 313) ; Sodium hydroxide (PubChem CID ; 14798)
• 刊名：Life Sciences
• 出版年：1 April, 2014
• 年：2014
• 卷：100
• 期：2
• 页码：138-146
• 全文大小：1081 K

文摘

Aims

尾-Adrenoceptors modulate acute wound healing; however, few studies have shown the effects of 尾-adrenoceptor blockade on chronic wounds. Therefore, this study investigated the effect of 尾₁-/尾₂-adrenoceptor blockade in wound healing of pressure ulcers.

Main methods

Male mice were daily treated with propranolol (尾₁-/尾₂-adrenoceptor antagonist) until euthanasia. One day after the beginning of treatment, two cycles of ischemia-reperfusion by external application of two magnetic plates were performed in skin to induce pressure ulcer formation.

Key findings

Propranolol administration reduced keratinocyte migration, transforming growth factor-尾 protein expression, re-epithelialization, and necrotic tissue loss. Neutrophil number and neutrophil elastase protein expression were increased in propranolol-treated group when compared with control group. Propranolol administration delayed macrophage mobilization and metalloproteinase-12 protein expression and reduced monocyte chemoattractant protein-1 protein expression. Myofibroblastic differentiation, angiogenesis, and wound closure were delayed in the propranolol-treated animals. Propranolol administration increased neo-epidermis thickness, reduced collagen deposition, and enhanced tenascin-C expression resulting in the formation of an immature and disorganized collagenous scar.

Significance

尾₁-/尾₂-Adrenoceptor blockade delays wound healing of ischemia-reperfusion skin injury through the impairment of the re-epithelialization and necrotic tissue loss which compromise wound inflammation, dermal reconstruction, and scar formation.