Protection of Human Corneal Epithelial Cells From TNF-α–Induced Disruption of Barrier Function by Rebamipide

Kimura, Kazuhiro; Morita, Yukiko; Orita, Tetsuji; Haruta, Junpei; Takeji, Yasuhiro; Sonoda, Koh Hei

doi:10.1167/iovs.12-11294

Cited by 73 publications

(52 citation statements)

References 49 publications

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“…The aim of this study was to evaluate taste-masking effect of CGA on bitter drugs using taste sensor measurements and surface plasmon resonance (SPR) analysis of CGA-drug interactions. Six different bitter drugs were used: amlodipine besylate (AMD), [19][20][21] diphenhydramine hydrochloride (DPH), 22) donepezil hydrochloride (DNP), 6) rebamipide (RBM), 18,23,24) diclofenac sodium (DCF) 25) and etodolac (ETD). 25) These drugs are well-established as bitter medicines and are widely used in clinical practice.…”

Section: Taste-masking Effect Of Chlorogenic Acid (Cga) On Bitter Drumentioning

confidence: 99%

Taste-Masking Effect of Chlorogenic Acid (CGA) on Bitter Drugs Evaluated by Taste Sensor and Surface Plasmon Resonance on the Basis of CGA–Drug Interactions

Shiraishi

Haraguchi

Nakamura

et al. 2017

CHEMICAL & PHARMACEUTICAL BULLETIN

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The purpose of this study was to evaluate the taste-masking effects of chlorogenic acid (CGA) on bitter drugs using taste sensor measurements and surface plasmon resonance (SPR) analysis of CGA-drug interactions. Six different bitter drugs were used: amlodipine besylate (AMD), diphenhydramine hydrochloride (DPH), donepezil hydrochloride (DNP), rebamipide (RBM), diclofenac sodium (DCF) and etodolac (ETD). Taste sensor outputs were significantly inhibited by the addition of CGA to all drugs. The inhibition ratio of the taste sensor output decreased in the following order DPH>DNP>AMD≈DCF≈RBM≈ETD. The association rate constant (k a ) for the interaction between drugs and CGA as evaluated by SPR measurement also decreased in the following order DPH>DNP>AMD>DCF≈ETD≈RBM. It was suggested that basic drugs (AMD, DNP, DPH) associate more easily with CGA than acidic drugs (DCF, RBM, ETD). The inhibition ratios (%) of the taste sensor output of bitter drugs caused by CGA and the association rate constants (k a ) between the drugs and CGA were significantly correlated (r s 0.886, p<0.05, Spearman's correlation test). Our findings suggest that the taste-masking effects of CGA are due to its direct association with the drugs. CGA may therefore be a useful taste-masking agent for basic drugs.

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Section: Taste-masking Effect Of Chlorogenic Acid (Cga) On Bitter Drumentioning

confidence: 99%

Taste-Masking Effect of Chlorogenic Acid (CGA) on Bitter Drugs Evaluated by Taste Sensor and Surface Plasmon Resonance on the Basis of CGA–Drug Interactions

Shiraishi

Haraguchi

Nakamura

et al. 2017

CHEMICAL & PHARMACEUTICAL BULLETIN

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“…It also causes a decrease in the secretion of inflammatory cytokines. A 2 % ophthalmic solution of rebamipide increases tear stability markedly and causes an increase in MUC5 mRNA expression on the ocular surface [97,98]. Ohguchi et al [99] have shown the anti-inflammatory effect of rebamipide on tears, as well as the antioxidant effect on the conjunctiva.…”

Section: Biological Agentsmentioning

confidence: 99%

“…Rebamipide also decreases cytokine expression in human corneal epithelium by treating the barrier dysfunction related to TNF-a [99]. Kimura et al have shown that rebamipide blocks the barrier dysfunction and protects Z01 expression [98].…”

Section: Biological Agentsmentioning

confidence: 99%

The role and treatment of inflammation in dry eye disease

Yağcı

Gürdal

2014

Int Ophthalmol

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Dry eye syndrome is a common ocular surface problem, affects 10-30 % of the population, especially in those who are older than 40 years. As a consequence of the demographic pressure created by the aging population, its prevalence is expected to increase as well as its burden on ophthalmologic practices. Thus, understanding the complex underlying mechanisms and development of thoughtful, effective strategies that involve these mechanisms are critical. Many factors causing ocular surface damage and inflammation have been shown to contribute to the etiopathogenesis. Increased osmolarity induces ocular surface inflammation leading to disruption of both the quality and quantity of tears. Pathologic tear function and the ocular surface inflammation affects the neural arcade and increases apoptosis in the ocular surface cells thus creating a viscous cycle for dry eye by causing unstable and hyperosmolar tears. Thus, the treatment objective is to prevent severe dry eye complications via preventing inflammation and apoptosis of the ocular surface cells. The ultimate target is a normalized ocular surface, increased tear stability, and decreased osmolarity of the tear film. In the light of current literature, this review aims to elucidate the role of inflammation as the main etiological factor in dry eye disease and discuss current therapeutic approaches to overcome it.

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“…Immunoblot analysis of total or phosphorylated forms of ERK, p38 MAPK, JNK, and IjB-a, as well as of RAR-a, RAR-b, and RAR-c, was also performed as described previously. 20 In brief, cells were lysed in a solution containing 50 mM Tris-HCl (pH 7.5), 150 mM NaCl, 1 mM EDTA, 5 mM NaF, 1% Nonidet P-40, 0.5% sodium deoxycholate, 0.1% SDS, 1 mM Na 3 VO 4 , and 1% protease inhibitor cocktail, and the cell lysates (10 lg protein) were subjected to immunoblot analysis.…”

Section: Immunoblot Analysismentioning

confidence: 99%

Suppression by an RAR-γ Agonist of Collagen Degradation Mediated by Corneal Fibroblasts

Kimura

Zhou

Orita

et al. 2017

Invest. Ophthalmol. Vis. Sci.

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PURPOSE.To examine the role of retinoic acid receptor (RAR) isoforms in interleukin-1b (IL1b)-induced collagen degradation by corneal fibroblasts.METHODS. Primary rabbit corneal fibroblasts embedded in a three-dimensional collagen gel were incubated with or without all-trans retinoic acid (ATRA), the RAR-a agonist Am580, the RAR-b agonist AC55649, or the RAR-c agonist R667. Collagen degradation was determined by measurement of hydroxyproline produced in acid hydrolysates of culture supernatants. Matrix metalloproteinase (MMP) expression was evaluated by immunoblot analysis and gelatin zymography. The phosphorylation of mitogen-activated protein kinases (MAPKs) and the endogenous nuclear factor (NF)-jB inhibitor IjB-a was examined by immunoblot analysis. Cell proliferation was measured with a bromodeoxyuridine incorporation assay, and cell viability was determined by measurement of the release of lactate dehydrogenase. RESULTS.Interleukin-1b-induced collagen degradation by corneal fibroblasts was inhibited by ATRA, Am580, and R667 in a concentration-dependent manner but was unaffected by AC55649, with the inhibitory effects of ATRA and R667 being markedly greater than that of Am580. The IL-1b-induced production of MMP-1, MMP-2, MMP-3, and MMP-9 by corneal fibroblasts was also inhibited by R667 in a concentration-dependent manner. R667 inhibited the IL-1b-induced phosphorylation of IjB-a but not that of MAPKs. R667 had no effect on the proliferation or viability of corneal fibroblasts.CONCLUSIONS. The RAR-c agonist R667 suppressed MMP production and thereby inhibited collagen degradation by corneal fibroblasts exposed to the proinflammatory cytokine IL-1b. These effects of R667 may be mediated by the NF-jB signaling pathway.

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Protection of Human Corneal Epithelial Cells From TNF-α–Induced Disruption of Barrier Function by Rebamipide

Cited by 73 publications

References 49 publications

Taste-Masking Effect of Chlorogenic Acid (CGA) on Bitter Drugs Evaluated by Taste Sensor and Surface Plasmon Resonance on the Basis of CGA–Drug Interactions

Taste-Masking Effect of Chlorogenic Acid (CGA) on Bitter Drugs Evaluated by Taste Sensor and Surface Plasmon Resonance on the Basis of CGA–Drug Interactions

The role and treatment of inflammation in dry eye disease

Suppression by an RAR-γ Agonist of Collagen Degradation Mediated by Corneal Fibroblasts

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