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

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To evaluate the influence of overexpression HGF on the healing of traumatic ulcer of oral mucosa of mice.

Material and methods

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 5 days 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.

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