METHODS: Ninety-six healthy C57/6J mice were randomly divided into blank control group, phosphate buffered solution(PBS)group and LC group. The blank control group did not receive any treatment, LC group and PBS group were prepared acute alkali burn models. LC group was given 60mmol/L LC eye drops, and PBS group was given PBS eye drops, 6 times/d, for continuous days from one day before alkali burn. The repair of corneal epithelium was observed by fluorescein sodium staining under slit lamp microscope at 0h, 3 and 7d. On the 3d, the expressions of Ki-67 and IL-1β proteins in cornea were detected by immunofluorescence, the total proteins of corneal epithelial were extracted for Western blot to detect the expression of P63, NLRP3, Caspase-1 and phosphorylation level of STAT3.

RESULTS: The results of corneal fluorescein sodium staining showed that on the 3 and 7d after alkali burn, the percentage of residual corneal epithelial defect area in PBS group compared with LC group was(29.38±6.83)% vs(17.78±4.11)% and(14.23±4.51)% vs(4.10±2.10)%, respectively(P<0.01). The repair of corneal epithelium in LC group was faster than that in PBS group. On the 3d, compared with the blank control group, the expressions of pyroptosis related proteins NLRP3 and Caspase-1 in the corneal epithelium of the alkali burn treated mice were up-regulated, the expression of P63 was decreased, and the p-STAT3/STAT3 level was increased, all the differences were significant except cleaved Caspase-1 of blank control group vs LC group. Compared with PBS group, in LC group, the expression of NLRP3, pro Caspase-1 and cleaved Caspase-1 protein were decreased, P63 was up-regulated, and p-STAT3 /STAT3 was increased, all the differences were significant. Immunofluorescence showed that compared with the blank control group,the expressions of IL-1β and Ki-67 were up-regulated in the alkali burned group. Compared with PBS group, the expression of Ki-67 protein was up-regulated and IL-1β was decreased in LC group.

CONCLUSION: LC can promote the proliferation of stem/progenitor cells in the corneal epithelium of mice and further promote the repair of corneal epithelium after alkali burn by inhibiting the pyroptosis signaling pathway and promoting the activation of STAT3 signaling pathway.