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Related Experiment Videos

ML-7, chelerythrine and phorbol ester increase outflow facility in the monkey Eye.

B Tian1, L C Brumback, P L Kaufman

  • 1Department of Ophthalmology and Visual Sciences, University of Wisconsin-Madison Medical School, Madison, WI 53792, USA.

Experimental Eye Research
|November 30, 2000
PubMed
Summary

Myosin light chain kinase (MLCK) and protein kinase C (PKC) inhibitors, ML-7 and chelerythrine (CHEL), significantly increased aqueous humor outflow facility in cynomolgus monkey eyes. Combined treatments with CHEL and PMA also enhanced outflow facility, suggesting a cytoskeletal mechanism.

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Area of Science:

  • Ocular Physiology
  • Pharmacology
  • Cell Biology

Background:

  • Aqueous humor outflow facility is crucial for maintaining intraocular pressure.
  • Myosin light chain kinase (MLCK) and protein kinase C (PKC) are implicated in regulating ocular tissues involved in aqueous humor outflow.

Purpose of the Study:

  • To investigate the effects of MLCK inhibitor ML-7 and PKC inhibitor chelerythrine (CHEL) on aqueous humor outflow facility in cynomolgus monkey eyes.
  • To determine the influence of PKC activator phorbol myristate acetate (PMA) and serine-threonine kinase inhibitor H-7 on outflow facility, both alone and in combination with ML-7 or CHEL.

Main Methods:

  • Constant pressure perfusion of the anterior chamber (AC) in cynomolgus monkey eyes.
  • Treatment with ML-7, CHEL, PMA, H-7, or their respective vehicles, followed by AC infusion.

Related Experiment Videos

  • Measurement of outflow facility at baseline and post-drug administration.

    • Main Results:

    • ML-7 and CHEL dose-dependently increased outflow facility.
    • CHEL demonstrated significant facility increases even at lower concentrations and over extended perfusion times.
    • H-7 potentiated the effects of ML-7 and CHEL.
    • PMA dose-dependently increased outflow facility, with combined CHEL and PMA showing synergistic effects at higher concentrations.

    Conclusions:

    • ML-7 and CHEL likely enhance outflow facility through a cytoskeletal mechanism.
    • PKC inhibition may not be the primary mechanism for the facility-increasing effects of CHEL and PMA.
    • These findings suggest potential therapeutic targets for managing intraocular pressure.