잠시만 기다려 주세요. 로딩중입니다.

Effect of Diquafosol on Hyperosmotic Stress-induced Tumor Necrosis Factor-α and Interleukin-6 Expression in Human Corneal Epithelial Cells

Korean Journal of Ophthalmology 2020년 34권 1호 p.1 ~ 10
김연희 ( Kim Yeoun-Hee ) - Myungmoon Bio

양인준 ( Yang In-Jun ) - Dongguk University College of Korean Medicine Department of Physiology
 ( Nguyen Ly Thi Huong ) - Dongguk University College of Korean Medicine Department of Physiology
 ( Gum Sang-Il ) - Binaree
 ( Yu Sung ) - Central Ophthalmic Clinic
이광자 ( Lee Gwang-Ja ) - Central Ophthalmic Clinic
김보애 ( Kim Bo-Ae ) - Mokwon University College of Sciences & Technology Division of Biomedicinal and Cosmetics
정재창 ( Jung Jae-Chang ) - Kyungpook National University College of Natural Sciences Department of Biology
박영정 ( Park Young-Jeung ) - Central Ophthalmic Clinic

Abstract


Purpose: Diquafosol is a pharmaceutical drug used for dry eye treatment with a novel mechanism of action. It is a purinergic P2Y2 receptor agonist that promotes the secretion of tears and healing of corneal epithelial wounds. However, its inhibitory effect on hyperosmotic stress-induced inflammation in human corneal epithelial cells (HCECs) remains unclear.

Methods: A hyperosmotic stress model was established by transferring HCECs from isosmotic (312 mOsm/kg to hyperosmotic medium (500 mOsm/kg). HCECs were incubated with 500 mOsm/kg hyperosmotic medium for 30 minutes, and then treated with diquafosol (0.6?6 mg/mL) for 4 or 24 hours. Cells were then harvested and analyzed by western blot, immunocytochemistry, and real-time polymerase chain reaction to evaluate the expression of interleukin-6, tumor necrosis factor-alpha, and the phosphorylation status of nuclear factor-kappa B.

Results: Diquafosol significantly decreased the mRNA and protein expression of hyperosmotic stress-induced tumor necrosis factor-alpha and interleukin-6. These results were supported by immunofluorescence staining and quantitative real-time polymerase chain reaction analysis. Furthermore, diquafosol inhibits nuclear factor-kappa B activation by suppressing the phosphorylation and degradation of the inhibitor of кB.

Conclusions: This study shows that diquafosol inhibits nuclear factor-kappa B signaling and inflammatory factors induced by hyperosmotic stress in HCECs. This suggests that using diquafosol for the improvement of dry eye syndrome could be effective in the treatment of inflammation-related corneal and conjunctival diseases.

키워드

Diquafosol; Human corneal epithelial cells; Inflammation; Interleukin-6; Tumor necrosis factor-alpha
원문 및 링크아웃 정보
  
등재저널 정보
MEDLINE
KCI
KoreaMed
KAMS