TY - JOUR
T1 - Characterization of the inhibitory effect of gastrodigenin and gastrodin on M-type K+ currents in pituitary cells and hippocampal neurons
AU - Yang, Chih Sheng
AU - Lai, Ming Chi
AU - Liu, Ping Yen
AU - Lo, Yi Ching
AU - Huang, Chin Wei
AU - Wu, Sheng Nan
N1 - Funding Information:
Department of Neurology, Taichung Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Taichung City 42743, Taiwan; yashchun@gmail.com Department of Pediatrics, Chi-Mei Medical Center, Tainan City 71004, Taiwan; vickylai621@gmail.com Department of Cardiology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan City 70101, Taiwan; larry@mail.ncku.edu.tw Department of Pharmacology, College of Medicine, Kaohsiung Medical University, Kaohsiung City 80708, Taiwan; yichlo@kmu.edu.tw Department of Neurology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan City 70101, Taiwan Department of Physiology, National Cheng Kung University Medical College, Tainan City 70101, Taiwan Institute of Basic Medical Sciences, National Cheng Kung University Medical College, Tainan City 70101, Taiwan Department of Medical Research, China Medical University Hospital, China Medical University, Taichung 40402, Taiwan Correspondence: huangcw@mail.ncku.edu.tw (C.-W.H.); snwu@mail.ncku.edu.tw (S.-N.W.); Tel.: +886-6-2353535-5334 (S.-N.W.)
Funding Information:
This research was funded in part by Taichung Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation (grant number: TTCRD107-05 to C.-S.Y.) and the National Cheng Kung University (grant numbers: D106-35A13 and NCKUH-10709001 to S.-N.W.).
Funding Information:
Funding: This research was funded in part by Taichung Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation (grant number: TTCRD107-05 to C.-S.Y.) and the National Cheng Kung University (grant numbers: D106-35A13 and NCKUH-10709001 to S.-N.W.) Acknowledgments: The authors would like to acknowledge the significant contribution that Kaisen Lee made to this work.
Publisher Copyright:
© 2019 by the authors. Licensee MDPI, Basel, Switzerland.
PY - 2020/1/1
Y1 - 2020/1/1
N2 - Gastrodigenin (HBA) and gastrodin (GAS) are phenolic ingredients found in Gastrodia elata Blume (GEB), a traditional Chinese herbal medicine. These compounds have been previously used to treat cognitive dysfunction, convulsion, and dizziness. However, at present, there is no available information regarding their potential ionic effects in electrically excitable cells. In the current study, the possible effects of HBA and GAS on different ionic currents in pituitary GH3 cells and hippocampal mHippoE-14 neurons were investigated using the patch-clamp technique. The addition of HBA or GAS resulted in the differential inhibition of the M-type K+ current (IK(M)) density in a concentration-dependent manner in GH3 cells. HBA resulted in a slowing of the activation time course of IK(M), while GAS elevated it. HBA also mildly suppressed the density of erg-mediated or the delayed-rectifier K+ current in GH3 cells. Neither GAS nor HBA (10 µM) modified the voltage-gated Na+ current density, although they suppressed the L-type Ca2+ current density at the same concentration. In hippocampal mHippoE-14 neurons, HBA was effective at inhibiting IK(M) density as well as slowing the activation time course. Taken together, the present study provided the first evidence that HBA or GAS could act on cellular mechanisms, and could therefore potentially have a functional influence in various neurologic disorders.
AB - Gastrodigenin (HBA) and gastrodin (GAS) are phenolic ingredients found in Gastrodia elata Blume (GEB), a traditional Chinese herbal medicine. These compounds have been previously used to treat cognitive dysfunction, convulsion, and dizziness. However, at present, there is no available information regarding their potential ionic effects in electrically excitable cells. In the current study, the possible effects of HBA and GAS on different ionic currents in pituitary GH3 cells and hippocampal mHippoE-14 neurons were investigated using the patch-clamp technique. The addition of HBA or GAS resulted in the differential inhibition of the M-type K+ current (IK(M)) density in a concentration-dependent manner in GH3 cells. HBA resulted in a slowing of the activation time course of IK(M), while GAS elevated it. HBA also mildly suppressed the density of erg-mediated or the delayed-rectifier K+ current in GH3 cells. Neither GAS nor HBA (10 µM) modified the voltage-gated Na+ current density, although they suppressed the L-type Ca2+ current density at the same concentration. In hippocampal mHippoE-14 neurons, HBA was effective at inhibiting IK(M) density as well as slowing the activation time course. Taken together, the present study provided the first evidence that HBA or GAS could act on cellular mechanisms, and could therefore potentially have a functional influence in various neurologic disorders.
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U2 - 10.3390/ijms21010117
DO - 10.3390/ijms21010117
M3 - Article
C2 - 31877994
AN - SCOPUS:85077255580
SN - 1661-6596
VL - 21
JO - International journal of molecular sciences
JF - International journal of molecular sciences
IS - 1
M1 - 117
ER -