Basic Research
Copyright ©The Author(s) 2004. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jan 1, 2004; 10(1): 96-99
Published online Jan 1, 2004. doi: 10.3748/wjg.v10.i1.96
Electrophysiological effects of anthopleurin-Q on rat hepatocytes
Hong-Yi Zhou, Fang Wang, Ke-Qiang Zhang, Lan Cheng, Ji Zhou, Li-Ying Fu, Wei-Xing Yao
Hong-Yi Zhou, Fang Wang, Lan Cheng, Ji Zhou, Li-Ying Fu, Wei-Xing Yao, Department of Pharmacology, Tongji Medical College of Huazhong University of Science and Technology, Wuhan 430030, Hubei Province, China
Ke-Qiang Zhang, Department of Infectious Diseases, Jianghan Oil Field Central Hospital, Qianjiang 433124, Hubei Province, China
Author contributions: All authors contributed equally to the work.
Correspondence to: Dr. Hong -Yi Zhou, Department of Pharmacology, Tongji Medical College of Huazhong University of Science and Technology, Wuhan 430030, Hubei Province, China. zhouhy518@yahoo.com.cn
Telephone: +86-27-83692033
Received: May 11, 2003
Revised: May 23, 2004
Accepted: June 2, 2003
Published online: January 1, 2004
Abstract

AIM: To study the effects of AP-Q on CCl4-induced acute liver injury, delayed outward potassium current (IK), inward rectifier potassium current (IK1) and calcium release-activated calcium current (ICRAC) in isolated rat hepatocytes.

METHODS: A single dose of CCl4 (10 μg/mL, ip) was injected to induce acute liver injury in rats. Serum aminotransferase activities were determined. Whole cell patch-clamp techniques were used to investigate the effects of AP-Q on delayed outward potassium current (IK), inward rectifier potassium current (IK1) and calcium release-activated calcium current (ICRAC).

RESULTS: AP-Q (3.5 and 7 μg/kg) pretreatment significantly reduced ALT and AST activities. AP-Q 0.1-100 nM produced a concentration-dependent increase of IK with EC50 value of 5.55±1.8 nM (n=6). AP-Q 30 nM shifted the I-V curve of IK leftward and upward. CCl4 4 mM decreased IK current 28.6±6.5% at 140 mV. After exposure to CCl4 for 5 min, AP-Q 30 nM attenuated the decrease of IK induced by CCl4 close to normal amplitude. AP-Q 0.01-100 nM had no significant effect on either inward or outward components of IK1 at any membrane potential examined. AP-Q 0.1-100 nM had no significant influence on the peak amplitude of ICRAC, either, and did not affect the shape of its current voltage curve.

CONCLUSION: AP-Q has a protective effect on CCl4-induced liver injury, probably through selectively increased IK in hepatocytes.

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