ArticleWorld journal of gastroenterology2004
Electrophysiological effects of anthopleurin-Q on rat hepatocytes.
Article in World journal of gastroenterology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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7 authors at 2 institutions in 1 country.
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Abstract
aimTo study the effects of AP-Q on CCl(4)-induced acute liver injury, delayed outward potassium current (I(K)), inward rectifier potassium current (I(K1)) and calcium release-activated calcium current (I(CRAC)) in isolated rat hepatocytes.
methodsA single dose of CCl(4) (10 microg/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 (I(K)), inward rectifier potassium current (I(K1)) and calcium release-activated calcium current (I(CRAC)).
resultsAP-Q (3.5 and 7 microg/kg) pretreatment significantly reduced ALT and AST activities. AP-Q 0.1-100 nM produced a concentration-dependent increase of I(K) with EC(50) value of 5.55+/-1.8 nM (n=6). AP-Q 30 nM shifted the I-V curve of I(K) leftward and upward. CCl(4) 4 mM decreased I(K) current 28.6+/-6.5% at 140 mV. After exposure to CCl(4) for 5 min, AP-Q 30 nM attenuated the decrease of I(K) induced by CCl(4) close to normal amplitude. AP-Q 0.01-100 nM had no significant effect on either inward or outward components of I(K1) at any membrane potential examined. AP-Q 0.1-100 nM had no significant influence on the peak amplitude of I(CRAC), either, and did not affect the shape of its current voltage curve.
conclusionAP-Q has a protective effect on CCl(4)-induced liver injury, probably through selectively increased I(K) in hepatocytes.
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