PMID- 9103534
OWN - NLM
STAT- MEDLINE
DCOM- 19970502
LR  - 20161124
IS  - 0022-3565 (Print)
IS  - 0022-3565 (Linking)
VI  - 281
IP  - 1
DP  - 1997 Apr
TI  - Preventive effect of rebamipide on gastric mucosal cell damage evoked by 
      activation of formyl-methionyl-leucyl-phenylalanine receptors of rabbit 
      neutrophils.
PG  - 478-83
AB  - We investigated the underlying mechanism by which rebamipide exerts a preventive 
      effect on neutrophil-mediated gastric mucosal cell damage. The release of 
      2',7'-bis-(2-carboxyethyl)-5-(and -6)-carboxyfluorescein (an index of 
      cytotoxicity) was significantly increased by 16.7% (P < .05) when 
      2',7'-bis-(2-carboxyethyl)-5-(and -6)-carboxyfluorescein-acetomethyl ester (5 
      microM) loaded gastric mucosal cells were incubated with neutrophils (5 x 10(6) 
      cells/well) that were activated by cytochalasin B (5 microM) and 
      formyl-methionyl-leucyl-phenylalanine (fMLP) (1 nM). In the in vitro study, upon 
      application of cytochalasin B and fMLP, formation of superoxide anion and release 
      of myeloperoxidase increased with increased neutrophil aggregation. These 
      parameters were attenuated by pretreatment with rebamipide (100-1000 microM) in a 
      concentration-dependent manner. In the Scatchard analysis, the maximum binding of 
      [3H]fMLP to neutrophils decreased from 0.57 to 0.44 pmol/2 x 10(6) cells (P < 
      .05) by application of rebamipide (300 microM) with little change in K(D). 
      Neutrophils isolated from rabbits orally treated with rebamipide (100 mg/kg for 3 
      days) also showed a decrease in the production of superoxide anion upon 
      stimulation with fMLP and a decrease in the binding of [3H]fMLP to its receptors 
      on the neutrophil plasma membrane (0.59-0.45 pmol/2 x 10(6) cells, P < .05). 
      Taken together, it is suggested that the inhibitory effect of rebamipide on the 
      neutrophil-mediated gastric mucosal cell injury is due, in part, to alterations 
      in the neutrophil membrane that ultimately result in a decrease in the number of 
      binding sites for fMLP to its receptors.
FAU - Kim, C D
AU  - Kim CD
AD  - Department of Pharmacology, College of Medicine, Pusan National University, 
      Korea.
FAU - Hong, K W
AU  - Hong KW
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Pharmacol Exp Ther
JT  - The Journal of pharmacology and experimental therapeutics
JID - 0376362
RN  - 0 (Anti-Ulcer Agents)
RN  - 0 (Quinolones)
RN  - 0 (Receptors, Formyl Peptide)
RN  - 0 (Receptors, Immunologic)
RN  - 0 (Receptors, Peptide)
RN  - 11062-77-4 (Superoxides)
RN  - 59880-97-6 (N-Formylmethionine Leucyl-Phenylalanine)
RN  - 8ZYQ1474W7 (Sodium Fluoride)
RN  - LR583V32ZR (rebamipide)
RN  - NI40JAQ945 (Tetradecanoylphorbol Acetate)
RN  - OF5P57N2ZX (Alanine)
SB  - IM
MH  - Alanine/*analogs & derivatives/toxicity
MH  - Animals
MH  - Anti-Ulcer Agents/*pharmacology
MH  - Dose-Response Relationship, Drug
MH  - Gastric Mucosa/*drug effects
MH  - N-Formylmethionine Leucyl-Phenylalanine/metabolism
MH  - Neutrophils/*drug effects/physiology
MH  - Quinolones/*toxicity
MH  - Rabbits
MH  - Receptors, Formyl Peptide
MH  - Receptors, Immunologic/*drug effects
MH  - Receptors, Peptide/*drug effects
MH  - Sodium Fluoride/pharmacology
MH  - Superoxides/metabolism
MH  - Tetradecanoylphorbol Acetate/pharmacology
EDAT- 1997/04/01 00:00
MHDA- 1997/04/01 00:01
CRDT- 1997/04/01 00:00
PHST- 1997/04/01 00:00 [pubmed]
PHST- 1997/04/01 00:01 [medline]
PHST- 1997/04/01 00:00 [entrez]
PST - ppublish
SO  - J Pharmacol Exp Ther. 1997 Apr;281(1):478-83.