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Rebamipide increases barrier function and attenuates TNFα-induced barrier disruption and cytokine expression in human corneal epithelial cells
  1. Hiroshi Tanaka1,
  2. Ken Fukuda2,
  3. Waka Ishida2,
  4. Yosuke Harada2,
  5. Tamaki Sumi2,
  6. Atsuki Fukushima2
  1. 1Machida Hospital, Kochi City, Kochi, Japan
  2. 2Department of Ophthalmology and Visual Science, Kochi Medical School, NankokuCity, Kochi, Japan
  1. Correspondence to Dr Ken Fukuda, Department of Ophthalmology and Visual Science, Kochi Medical School, Kohasu, Oko-cho, Nankoku City, Kochi 783-8505, Japan; k.fukuda{at}


Background Disruption of corneal epithelial barrier function by inflammation may contribute to the development of dry eye. The effects of rebamipide, a drug used for the treatment of dry eye, on barrier function and cytokine expression in a human corneal epithelial (HCE) cell line were examined.

Methods Barrier function of HCE cells was evaluated by measurement of transepithelial electrical resistance (TER). The subcellular localisation of the tight junction protein zonula occludens (ZO)-1 was examined by immunofluorescence analysis. The release of cytokines was determined with ELISAs, and the intracellular abundance of cytokine mRNAs was quantitated by reverse transcription and real-time PCR analysis. Degradation of the nuclear factor-κB inhibitor IκBα was detected by immunoblot analysis.

Results Rebamipide increased TER of HCE cells in a concentration-dependent manner as well as attenuating the loss of TER and the disappearance of ZO-1 from the cell surface induced by tumour necrosis factor α (TNFα). Rebamipide also suppressed TNFα-induced expression of interleukin-6 and interleukin-8 at the mRNA and protein levels and inhibited the TNFα-induced degradation of IκBα.

Conclusions The upregulation of barrier function and the anti-inflammatory effects of rebamipide, together with its mucin secretagogue activity, may contribute to the effectiveness of this drug for the treatment of dry eye.

  • Ocular surface
  • Tears
  • Drugs
  • Experimental &#8211 laboratory
  • Inflammation

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