Hepatocyte growth factor (HGF) optimizes oral traumatic ulcer healing of mice by reducing inflammation.

To evaluate the influence of overexpression HGF on the healing of traumatic ulcer of oral mucosa of mice. Mice were divided into two groups: wild type C57BL6(WT) and HGF high expression transgenic (HGF-Tg) mice. Traumatic ulcer of all mice were made by number 15 scalpel blade. Mice were sacrificed after 5days and the inflammation score and expression of TNFα, IFNγ, c-Met, apoptosis (TUNEL) and 40 serum inflammation cytokines were estimated. HGF-Tg mice presented a lower inflammation score (p=0.011), Serum TNFα expression in HGF-Tg ulcers is 1.3 times than WT ulcer and the difference is statistical significance (t test, p=0.003). Serum c-Met protein in HGF-Tg mice were significantly higher than WT mice (t test, p=0.004). No statistical difference was observed in the serum IFNγ between WT ulcer and HGF-Tg ulcer (t test, p=0.268). TNFα positive cytoplasm expression cells in connective tissue of HGF-Tg mice is significantly lower than that of WT group (t test, p=0.029). C-Met positive cytoplasm expression cells in both epithelium and connective tissue of HGF-Tg group is significantly higher than that of WT group (t test, p=0.040, p=0.000). Samples in HGF-Tg group showed a lower number of positive cells of epithelium TUNEL staining compared with that in the WT group (t test, p=0.035). HGF exhibited anti-inflammatory potential in oral traumatic ulcer through the reduction of epithelial apoptosis, connective tissue TNFα expression and induction of c-Met expression.