Adachi Y, Kamisako T
Second Department of Internal Medicine, Kinki University School of Medicine, Japan.
Nihon Rinsho. 1996 Mar;54(3):788-93.
Various effects of cholestatic drugs, bile acids, and estrogens on the hepatocyte plasma membranes, as well as their changes in the cholestatic diseases are briefly reviewed. Cyclosporin A inhibits bile salt transporter (BST) on the canalicular membrane (CM). Ethynylestradiol reduces canalicular glutathione excretion. Estradiol-17beta-D-glucuronide interacts with MDR1, and taurochenodeoxycholic acid and lithocholate-3-O-glucuronide may interact with vesicular transport system, each of which may relate with the genesis of cholestasis. In Byler disease, biliary chenodeoxycholic acid excretion is defective. Lipopolysaccharide decreases the function of canalicular multispesific organic anion transporter (MOAT) which seems the first step in septic cholestasis. Obstructive jaundice causes reduced activity of both canalicular BST and MOAT. The mechanisms of choleretic action of S-adenosylmethionine and other drugs are also reviewed.
本文简要综述了胆汁淤积性药物、胆汁酸和雌激素对肝细胞膜的各种作用，以及它们在胆汁淤积性疾病中的变化。环孢素A抑制胆小管膜（CM）上的胆盐转运体（BST）。乙炔雌二醇减少胆小管谷胱甘肽排泄。雌二醇-17β-D-葡萄糖醛酸与多药耐药蛋白1（MDR1）相互作用，牛磺鹅去氧胆酸和石胆酸-3-O-葡萄糖醛酸可能与囊泡转运系统相互作用，每一种都可能与胆汁淤积的发生有关。在布勒病中，胆汁鹅去氧胆酸排泄存在缺陷。脂多糖降低胆小管多特异性有机阴离子转运体（MOAT）的功能，这似乎是脓毒症性胆汁淤积的第一步。梗阻性黄疸导致胆小管BST和MOAT的活性降低。还综述了S-腺苷甲硫氨酸和其他药物的利胆作用机制。
