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Takikawa H, Sano N, Takada Y, et al. Effect of bile acids on biliary excretion of cyclosporin A in the rat. Hepatol Res. 2001;20(1):128-132doi: 10.1016/s1386-6346(00)00126-1.
Takikawa, H., Sano, N., Takada, Y., Toda, A., Tanaka, H., & Takamori, Y. (2001). Effect of bile acids on biliary excretion of cyclosporin A in the rat. Hepatology research : the official journal of the Japan Society of Hepatology, 20(1), 128-132. https://doi.org/10.1016/s1386-6346(00)00126-1
Takikawa, H, et al. "Effect of bile acids on biliary excretion of cyclosporin A in the rat." Hepatology research : the official journal of the Japan Society of Hepatology vol. 20,1 (2001): 128-132. doi: https://doi.org/10.1016/s1386-6346(00)00126-1
Takikawa H, Sano N, Takada Y, Toda A, Tanaka H, Takamori Y. Effect of bile acids on biliary excretion of cyclosporin A in the rat. Hepatol Res. 2001 May 01;20(1):128-132. doi: 10.1016/s1386-6346(00)00126-1. PMID: 11282491.
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Hepatol Res. 2001 May 01;20(1):128-132. doi: 10.1016/s1386-6346(00)00126-1.

Effect of bile acids on biliary excretion of cyclosporin A in the rat.

Hepatology research : the official journal of the Japan Society of Hepatology

H Takikawa, N Sano, Y Takada, A Toda, H Tanaka, Y Takamori

Affiliations

  1. Department of Medicine, Teikyo University School of Medicine, Kaga 2-11-1, Itabashi-ku, 173-8605, Tokyo, Japan

PMID: 11282491 DOI: 10.1016/s1386-6346(00)00126-1

Abstract

Cyclosporin A, a substrate of P-glycoprotein (P-gp), is known to cause cholestasis in humans and in rat experimental models. Tauroursodeoxycholate is reported to be effective in CyA-induced cholestasis in rats. In the present study, to investigate the mechanism of the inhibition of CyA induced cholestasis, effect of bile acids on biliary cyclosporin A excretion was studied in rats. Infusion of both taurocholate and tauroursodeoxycholate at the rate of 0.8 mmol/min per 100 g bodyweight increased bile flow and biliary cyclosporin A excretion, and the extent was more prominent with tauroursodeoxycholate. It was suggested that these findings were caused by the enhanced vesicular targeting of P-gp to the canalicular membrane by bile acids, thus increasing the numbers of P-gp in the canalicular membrane.

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