Histological and Molecular Biological Mechanisms of Pressure Therapy on Hypertrophic Scar

It was to investigate the histological and molecular mechanism of pressure therapy on hypertrophic scar (HS). HS animal model was established. A total of 63 male Sprague–Dawley rats were randomly rolled into blank group (BG, no modeling), control group (CG, modeling), and test group (TG, modeling and pressure therapy), with 21 rats in each group. Hypertrophic scar animal model was induced by heat burn, and hematoxylin and eosin (H&E) and Masson staining were performed on the skin tissues of rat. mRNA levels and protein expression levels of vascular endothelial growth factor (VEGF), insulin-like growth factor (IGF), IGF 1 receptor (IGF1R), and MEK2 signaling pathway were detected by quantitative PCR (qPCR) and Western blotting. After the pressure therapy, the collagen fibers in the skin tissues of the rat in TG returned to regular arrangement, and the fibroblasts were arranged orderly. On the 28th day, the mRNA levels of IGF-1 and VEGF in TG greatly surpassed CG (P < 0.05), mRNA expression levels of IGF-1R, PI3K, MEK2, and ERK2 were lower than CG (P < 0.05), and PI3K protein expression levels were higher than CG (P < 0.05). The AKT2 protein expression levels in TG on the 28th and 35th days differed slightly versus CG (P > 0.05). On the 28th day, MEK2 protein expression levels in TG were lower than CG (P < 0.01), and MEK2 protein expression levels were higher on the 35th day (P < 0.05). The ERK2 protein expression levels in TG were lower than CG on 28th day and 35th day (P < 0.05), while VEGF protein expression levels were higher than CG (P < 0.05). Stress therapy effectively inhibited the formation of hypertrophic scars (HS) by significantly downregulating the expression of the MEK/ERK signaling pathway while concurrently upregulating VEGF expression. Furthermore, stress therapy alleviated the pathological process of HS by downregulating the expression of the IGF-1/IGF-1R signaling pathway and its downstream PI3K/AKT signaling cascade. These results suggest that stress therapy plays a crucial role in regulating the molecular mechanisms underlying HS formation.