Bile-salt hydrophobicity is a key factor regulating rat liver plasma-membrane communication: relation to bilayer structure, fluidity and transporter expression and function

Bile-salt hydrophobicity is a key factor regulating rat liver plasma-membrane communication: relation to bilayer structure, fluidity and transporter expression and function
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DOI:
10.1042/0264-6021:3590605
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发表时间:
2001-11-01
影响因子:
4.1
通讯作者:
Suzuki, H
Suzuki, H
中科院分区:
生物学3区
文献类型:
--
作者:
Asamoto, Y;Tazuma, S;Suzuki, H

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胆盐疏水性调节胆汁磷脂分泌和亚选择。本研究的目的是确定胆盐是否可以影响肝细胞膜磷脂和流动性的ATP依赖性转运蛋白。通过过夜胆汁分流耗尽大鼠的胆汁盐,然后以恒定速率(200 nmol/min/100 g体重)静脉输注牛磺胆酸钠,随后输注具有各种疏水性的胆汁盐(牛磺鹅脱氧胆酸盐、牛磺熊脱氧胆酸盐、牛磺β-鼠胆酸盐、牛磺α-鼠胆酸盐,以200 nmol/min/100 g体重)。输注胆汁盐的疏水性与胆汁磷脂的疏水性相关,但与小管膜双层的疏水性呈负相关。小管膜流动性(估计1,6-二苯基-1,3,5-己三烯荧光去极化)和多药耐药蛋白(Mrp 2,Mrp 3)和顶端Na+依赖性胆盐转运蛋白(ASBT)的表达增加亲水性胆盐,虽然P-糖蛋白亚家族(Mdr 2)的表达没有显着变化。胆盐输出泵(Bsep)的表达随着胆盐疏水性的增加而沿着增加。胆盐调节小管膜磷脂和膜流动性,以及ATP依赖性转运蛋白的表达和功能,这些作用与其疏水性有关。亲水性胆汁盐的细胞保护作用似乎与诱导Mrp 2、Mrp 3和ASBT有关。
Bile-salt hydrophobicity regulates biliary phospholipid secretion and subselection. The aim of this study was to determine whether bile salts can influence liver plasma membrane phospholipids and fluidity in relation to the ATP-dependent transporter. Rats were depleted of bile salts by overnight biliary diversion and then sodium taurocholate was infused intravenously at a constant rate (200 nmol/min per 100 g of body weight), followed by infusion of bile salts with various hydrophobicities (taurochenodeoxy-cholate, tauroursodeoxycholate, tauro-beta -muricholate, tauro-alpha -muricholate at 200 nmol/min per 100 g of body weight). The hydrophobicity of the infused bile salts correlated with that of biliary phospholipids, but was inversely related to that of the canalicular membrane bilayer. Canalicular membrane fluidity (estimated by 1,6-diphenyl-1,3,5-hexatriene fluorescence depolarization) and expression of multidrug-resistance proteins (Mrp2, Mrp3) and apical Na+-dependent bile-salt transporter (ASBT) were increased by hydrophilic bile salts, although there was no marked change in the expression of P-glycoprotein subfamilies (Mdr2). Bile-salt export pump (Bsep) expression was increased along with increasing bile-salt hydrophobicity. Bile salts modulate canalicular membrane phospholipids and membrane fluidity, as well as the ATP-dependent transporter expression and function, and these actions are associated with their hydrophobicity. The cytoprotective effect of hydrophilic bile salts seems to be associated with induction of Mrp2, Mrp3 and ASBT.