Abstract:

Objective

To observe the therapeutic effect of recombinant human acidic fibroblast growth factor （rhaFGF） on acute wounds in diabetes mellitus （DM） mice， and to explore its possible underlying mechanisms in chronicity of acute DM wound.

Methods

Acute DM wound models were established in male C57 mice.The mice were divided into four groups： Con （n=17）， Con+rhaFGF （n=17）， DM（n=17）， and DM+rhaFGF （n=17）.rhaFGF （0.08 μg/cm²） or PBS was daily administered on wound surface for 14 days after wound creation.The wound healing rates were calculated in each group.On the 7th day after rhaFGF administration， the levels of IL-6 and TNF-α in serum and tissues of mice were detected by ELISA.Additionally， the expression of IL-1β， IL-18 and NLRP3 inflammatory-associated molecules （NLRP3， ASC，and Caspase-1） in the tissues were measured using Western blot analysis.

Results

From the 9th day after modeling， the wound healing rates observed in the DM group was significantly lower than those of the Con group （P＜0.05）.Additionally， the healing rates in the DM+ rhaFGF group was significantly higher than that in the DM group from the 7th day （P＜0.05）.On the 7th day after modeling， the levels of IL-6 and TNF-α in the DM group were significantly higher than those in the Con group.In contrast， the levels of these molecules in the DM + rhaFGF group were significantly lower than those in the DM group （P＜0.05）.The levels of NLRP3， ASC， caspase-1， IL-1β， and IL-18 in the tissues of the DM group were significantly higher than those in the Con group.In contrast， the levels of these molecules in the DM + rhaFGF group were significantly lower than those in the DM group （P＜0.05）.

Conclusion

RhaFGF promotes the healing of acute DM wounds by reducing the release of pro - inflammatory factors and preventing the transition from acute to chronic inflammation.This mechanism may be associated with the inhibition of NLRP3 in acute DM wounds.

Key words: Recombinant human acidic fibroblast growth factor, Diabetes mellitus, Acute trauma, Inflammation, NLRP3