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Related Experiment Videos

Irsogladine inhibits ionomycin-induced decrease in intercellular communication in cultured rabbit gastric epithelial

Y Kameda1, F Ueda

  • 1Research Laboratories, Nippon Shinyaku Co., Ltd., Kyoto, Japan.

Japanese Journal of Pharmacology
|November 1, 1995
PubMed
Summary
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Irsogladine prevents ionomycin from disrupting intercellular communication and increasing intracellular calcium (Ca2+) in gastric cells. This suggests irsogladine may suppress calcium release from internal stores, maintaining cell communication.

Area of Science:

  • Cell Biology
  • Pharmacology

Background:

  • Intercellular communication is vital for tissue function.
  • Calcium ions (Ca2+) play a critical role in cellular signaling.
  • Gastric epithelial cells form a crucial barrier and require intact communication.

Purpose of the Study:

  • To investigate the effects of irsogladine on ionomycin-induced changes in intercellular communication and intracellular calcium levels.
  • To explore the role of intracellular calcium stores in ionomycin-induced disruption of cell communication.

Main Methods:

  • Cultured rabbit gastric epithelial cells were used.
  • Cells were treated with ionomycin to induce changes in intercellular communication and intracellular Ca2+.
  • The effects of irsogladine and TMB-8 on these ionomycin-induced changes were assessed.

Related Experiment Videos

  • Experiments were conducted with and without extracellular calcium.

    • Main Results:

    • Ionomycin decreased intercellular communication and increased intracellular Ca2+ in a concentration-dependent manner.
    • Irsogladine (10(-5) M) suppressed these ionomycin-induced effects, independent of extracellular Ca2+.
    • TMB-8 (10(-6) M) also suppressed the ionomycin-induced elevation of intracellular Ca2+ and decrease in intercellular communication.

    Conclusions:

    • The ionomycin-induced decrease in intercellular communication is likely caused by the mobilization of Ca2+ from intracellular stores.
    • Irsogladine and TMB-8 may exert their protective effects by inhibiting this intracellular Ca2+ mobilization.