摘要

Purpose This study assessed the anti-inflammatory effect and mechanism of action of hinokitiol in human corneal epithelial (HCE) cells. @@@ Methods HCE cells were incubated with different concentrations of hinokitiol or dimethylsulfoxide (DMSO), which served as a vehicle control. Cell viability was evaluated using Cell Counting Kit-8 (CCK-8) assay. After polyriboinosinic: polyribocytidylic acid (poly(I:C)) stimulus, cells with or without hinokitiol were evaluated for the mRNA and protein levels of interleukin-8 (IL-8), interleukin-6 (IL-6), and interleukin-1 beta (IL-1 beta) using real-time PCR analysis and an enzyme-linked immunosorbent assay (ELISA), respectively. Nuclear and cytoplasmic levels of nuclear factor kappa B (NF-kappa B) p65 protein and an inhibitor of NF-kappa B alpha (I kappa B alpha) were evaluated using western blotting. @@@ Results There were no significant differences among the treatment concentrations of hinokitiol compared with cells incubated in medium only. Incubating with 100 mu M hinokitiol significantly decreased the mRNA levels of IL-8 to 58.77 +/- 10.41% (P < 0.01), IL-6 to 64.64 +/- 12.71% (P < 0.01), and IL-1 beta to 54.19 +/- 8.10% (P < 0.01) compared with cells stimulated with poly(I:C) alone. The protein levels of IL-8, IL-6, and IL-1 beta had similar trend. Further analysis revealed that hinokitiol maintained the levels of I kappa B alpha and significantly reduced NF-kappa B p65 subunit translocation to the nucleus which significantly inhibiting the activation of the NF-kappa B signal pathway. @@@ Conclusion Hinokitiol showed a significant protective effect against ocular surface inflammation through inhibiting the NF-kappa B pathway, which may indicate the possibility to relieve the ocular surface inflammation of dry eye syndrome (DES).