Stimulatory actions of caffeic acid phenethyl ester, a known inhibitor of NF-κB activation, on Ca2+-activated K+ current in pituitary GH3 cells

Ming Wei Lin, Su Rong Yang, Mei Han Huang, Sheng-Nan Wu

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

Caffeic acid phenethyl ester (CAPE), a phenolic antioxidant derived from the propolis of honeybee hives, is known to be an inhibitor of activation of nuclear transcript factor NF-κB. Its effects on ion currents have been investigated in pituitary GH3 cells. This compound increased Ca 2+-activated K+ current (IK(Ca)) in a concentration-dependent manner with an EC50 value of 14 ± 2 μm. However, the magnitude of CAPE-induced stimulation of IK(Ca) was attenuated in GH3 cells preincubated with 2,2′-azo-bis-(2- amidinopropane) hydrochloride (100 μM) pm) or t-butyl hydroperoxide (1 mM). CAPE (50 μM) slightly suppressed voltage-dependent L-type Ca2+ current. In inside-out configuration, CAPE (20 μM) applied to the intracellular face of the detached patch enhanced the activity of large conductance Ca2+-activated K+ (BKCa) channels with no modification in single-channel conductance. After BKCa channel activity was increased by CAPE (20 μM), subsequent application of nordihydrogualaretic acid (20 μM) did not further increase the channel activity. CAPE-stimulated channel activity was dependent on membrane potential. CAPE could also increase Ca2+ sensitivity of BKCa channels in these cells. Its increase in the open probability could primarily involve a decrease in the mean closed time. In current-clamp conditions, CAPE hyperpolarized the membrane potential and reduced the firing of action potentials. The stimulatory effects on these channels may partly contribute to the underlying mechanisms through which this compound influences the functional activities of neurons or neuroendocrine cells. Caution has to be used in attributing its response in the activation of NF-κB.

Original languageEnglish
Pages (from-to)26885-26892
Number of pages8
JournalJournal of Biological Chemistry
Volume279
Issue number26
DOIs
Publication statusPublished - 2004 Jun 25

Fingerprint

Chemical activation
Membrane Potentials
Propolis
Membranes
tert-Butylhydroperoxide
Calcium-Activated Potassium Channels
Neuroendocrine Cells
caffeic acid phenethyl ester
Urticaria
Clamping devices
Action Potentials
Neurons
Antioxidants
Ions
Acids
Electric potential

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

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title = "Stimulatory actions of caffeic acid phenethyl ester, a known inhibitor of NF-κB activation, on Ca2+-activated K+ current in pituitary GH3 cells",
abstract = "Caffeic acid phenethyl ester (CAPE), a phenolic antioxidant derived from the propolis of honeybee hives, is known to be an inhibitor of activation of nuclear transcript factor NF-κB. Its effects on ion currents have been investigated in pituitary GH3 cells. This compound increased Ca 2+-activated K+ current (IK(Ca)) in a concentration-dependent manner with an EC50 value of 14 ± 2 μm. However, the magnitude of CAPE-induced stimulation of IK(Ca) was attenuated in GH3 cells preincubated with 2,2′-azo-bis-(2- amidinopropane) hydrochloride (100 μM) pm) or t-butyl hydroperoxide (1 mM). CAPE (50 μM) slightly suppressed voltage-dependent L-type Ca2+ current. In inside-out configuration, CAPE (20 μM) applied to the intracellular face of the detached patch enhanced the activity of large conductance Ca2+-activated K+ (BKCa) channels with no modification in single-channel conductance. After BKCa channel activity was increased by CAPE (20 μM), subsequent application of nordihydrogualaretic acid (20 μM) did not further increase the channel activity. CAPE-stimulated channel activity was dependent on membrane potential. CAPE could also increase Ca2+ sensitivity of BKCa channels in these cells. Its increase in the open probability could primarily involve a decrease in the mean closed time. In current-clamp conditions, CAPE hyperpolarized the membrane potential and reduced the firing of action potentials. The stimulatory effects on these channels may partly contribute to the underlying mechanisms through which this compound influences the functional activities of neurons or neuroendocrine cells. Caution has to be used in attributing its response in the activation of NF-κB.",
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Stimulatory actions of caffeic acid phenethyl ester, a known inhibitor of NF-κB activation, on Ca2+-activated K+ current in pituitary GH3 cells. / Lin, Ming Wei; Yang, Su Rong; Huang, Mei Han; Wu, Sheng-Nan.

In: Journal of Biological Chemistry, Vol. 279, No. 26, 25.06.2004, p. 26885-26892.

Research output: Contribution to journalArticle

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AU - Lin, Ming Wei

AU - Yang, Su Rong

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N2 - Caffeic acid phenethyl ester (CAPE), a phenolic antioxidant derived from the propolis of honeybee hives, is known to be an inhibitor of activation of nuclear transcript factor NF-κB. Its effects on ion currents have been investigated in pituitary GH3 cells. This compound increased Ca 2+-activated K+ current (IK(Ca)) in a concentration-dependent manner with an EC50 value of 14 ± 2 μm. However, the magnitude of CAPE-induced stimulation of IK(Ca) was attenuated in GH3 cells preincubated with 2,2′-azo-bis-(2- amidinopropane) hydrochloride (100 μM) pm) or t-butyl hydroperoxide (1 mM). CAPE (50 μM) slightly suppressed voltage-dependent L-type Ca2+ current. In inside-out configuration, CAPE (20 μM) applied to the intracellular face of the detached patch enhanced the activity of large conductance Ca2+-activated K+ (BKCa) channels with no modification in single-channel conductance. After BKCa channel activity was increased by CAPE (20 μM), subsequent application of nordihydrogualaretic acid (20 μM) did not further increase the channel activity. CAPE-stimulated channel activity was dependent on membrane potential. CAPE could also increase Ca2+ sensitivity of BKCa channels in these cells. Its increase in the open probability could primarily involve a decrease in the mean closed time. In current-clamp conditions, CAPE hyperpolarized the membrane potential and reduced the firing of action potentials. The stimulatory effects on these channels may partly contribute to the underlying mechanisms through which this compound influences the functional activities of neurons or neuroendocrine cells. Caution has to be used in attributing its response in the activation of NF-κB.

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