Mechanism of promoting wound healing by modified autologous blood transfusion in diabetic mice: relationship with MALAT1 / 中华麻醉学杂志

ABSTRACT

Objective:To evaluate the relationship between the mechanism of promoting wound healing by modified autologous blood transfusion and metastasis-associated lung adenocarcinoma transcript 1 ( MALAT1) in diabetic mice. Methods:Twenty SPF ICR mice, weighing 21-25 g, in which the diabetic model was successfully established, were divided into 2 groups ( n=10 each) using a random number table method: modified preservation group (group I) and ordinary preservation group (group O). Peripheral venous blood samples were collected and stored in the corresponding preservation solution for 7 days.The platelet aggregation rate, blood glucose, serum glycosylated hemoglobin (GHB) and phosphodiesterase (DPG) concentrations and WBC were measured.Autologous blood was transfused back immediately after the wound model was established.The percentage of wound healing area was calculated at 7, 10 and 14 days after autologous blood transfusion.The expression of hypoxia-inducible factor-1α, vascular endothelial growth factor, matrix metalloproteinase-9, β-actin, type Ⅰ collagen (Col Ⅰ), Col Ⅲ protein and mRNA and MALAT1 was determined by Western blot, immunohistochemistry and quantitative real-time polymerase chain reaction respectively, at 14 days after transfusion. Results:Compared with group O, the blood glucose, serum concentrations of GHB and DPG, and WBC were significantly decreased, platelet aggregation rate was increased, the percentage of wound healing area was increased, the positive staining rate of Col Ⅰ and Col Ⅲ was increased, and the expression of hypoxia-inducible factor-1α, vascular endothelial growth factor, matrix metalloproteinase-9, ColⅠ, Col Ⅲ and β-actin protein and mRNA and MALAT1 was up-regulated in group I ( P<0.05). Conclusion:The mechanism by which modified autologous blood transfusion promotes wound healing may be related to up-regulating MALAT1 expression in diabetic mice.