Corticosteroids modulate the secretory processes of the rat intrahepatic biliary epithelium

被引:41
|
作者
Alvaro, D
Gigliozzi, A
Marucci, L
Alpini, G
Barbaro, B
Monterubbianesi, R
Minetola, L
Mancino, MG
Medina, JF
Attili, AF
Benedetti, A
机构
[1] Univ Roma La Sapienza, Dept Clin Med, Div Gastroenterol, I-00185 Rome, Italy
[2] Univ Ancona, Dept Gastroenterol, Ancona, Italy
[3] Scott & White Mem Hosp & Clin, Dept Internal Med & Med Physiol, Temple, TX 76508 USA
[4] Texas A&M Univ, Coll Med, Temple, TX 76508 USA
[5] Cent Vet Hlth Care, Temple, TX USA
[6] Univ Navarra, Div Hepatol & Gene Therapy, Mol Genet Lab, E-31080 Pamplona, Spain
关键词
D O I
10.1053/gast.2002.32374
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background & Aims: We investigated the expression of glucocorticoid receptors (GcRs) in the intrahepatic biliary epithelium and the role of corticosteroids in the regulation of cholangiocyte secretion. Methods: GcR was studied by immunohistochemistry, reverse-transcription polymerase chain reaction, and Western blots. The effects of dexamethasone and budesonide on billary bicarbonate excretion and H+/HCO3- transport processes were investigated in bile fistula rats, isolated intrahepatic bile duct units (IBDUs), and purified cholangiocytes. Results: GcRs were expressed by rat cholangiocytes. Although acute administration of corticosteroids showed no effect, treatment for 2 days with dexamethasone or budesonide increased (P < 0.05) biliary bicarbonate concentration and secretion, which were blocked by the specific GcR antagonist, RU-486. IBDUs isolated from rats treated with dexamethasone or budesonide showed an increased (P < 0.05) activity of the Na+/H+ exchanger (NHE1 isoform) and Cl-/HCO3- exchanger (AE2 member), which was blocked by RU-486. Protein expression of NHE1 and AE2 and messenger RNA for NH1 but not AE2 were increased (P < 0.05) in isolated cholangiocytes by dexamethasone treatment. Conclusions: The intrahepatic biliary epithelium expresses GcR and responds to corticosteroids by increasing bicarbonate excretion in bile. This is caused by corticosteroid-induced enhanced activities and protein expression of transport processes driving bicarbonate excretion in the biliary epithelium.
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页码:1058 / 1069
页数:12
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