805 Inhibitory effect of tranexamic acid on UVB-induced inflammation in Hacat cells

      Chloasma is induced and aggravated by an important cause-radiation. UV radiation causes keratinocytes to secrete MMP-9 and HMGB-1, via inflammation, which can degrade collagen type 4. The exact mechanism of tranexamic acid(TA) in the treatment if chloasma is not yet clear. The query is whether it is related to the inhibition of local inflammation and MMPs. The cultured human skin keratinocytes (HaCaT cells) was divided into the control group, the Ultraviolet Radiation B(UVB)group, the UVB+TA group, the UVB+High mobility group box-l protein(HMGB1) inhibitor group and the UVB+Toll like receptor 4 (TLR-4) inhibitor group. In the preparation group, 10umol/l GA and CIL-095 were added respectively, and 50 mJ/cm2 UVB irradiation was applied in the irradiated group. At timepoints of 0h, 0.5h, 2h, 6h, immunofluorescence was used to observe the release of HMGB-1, and the optimal time (6h) was selected according to the immunofluorescence results. Western blotting was used to detect p-p38 MAP kinase(p-p38) expression in HaCaT cells. We found that UVB promotes MMP-9 secretion in Hacat cells. It has been found that the levels of MMP-9 in 25mJ/cm group and 50mJ/cm group were higher than that in the control group when detected the level of MMP-9 in cell supernatant 24 hours later. While TA inhibits UVB-induced MMP-9 secretion in Hacat cells. MMP-9 in cell supernatant of UVB group was significantly higher than the control group(P < 0.05); MMP-9 in cell supernatant of UVB+TA group was lower than that of UVB group (P < 0.05); there was no significant difference between single administration and control group. TA inhibits UVB-induced MMP-9 secretion in Hacat cells via TLR-4/p38 signaling pathway, and MMP-9 in the group of UVB+CIL-095 was lower than that in the group of UVB(P < 0.05). In conclusion, tranexamic acid can effectively inhibit UVB -induced MMP-9 and HMGB-1 secretion in Hacat cells via TLR-4/p38 signaling pathway.