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1 Department of Medical Physiology, Texas A&M University HSC, COM, Temple, TX, USA
2 Department of Internal Medicine, Scott and White Memorial Hospital, Temple, TX, USA
3 Department of Research and Education, Scott and White Memorial Hospital, Temple, TX, USA
4 Division of Gastroenterology, Tohoku University School of Medicine, Seiryo, Aobaku, Japan
5 Division of Gastroenterology, University of Rome, Rome, Japan
6 Department of Gastroenterology, University of Ancona, Ancona, Italy
7 Department of Public Health, University of Rome Tor Vergata, Rome, Italy
8 Department of Internal Medicine, Scott and White Memorial Hospital, Temple, TX, USA; Department of Research, Central Texas Veterans Health Care System, Temple, Texas, USA; Department of Medical Physiology, Texas A&M University HSC, COM, Temple, TX, USA
* To whom correspondence should be addressed. E-mail: galpini{at}tamu.edu.
Aim: to determine if taurocholate prevents vagotomy-induced cholangiocyte apoptosis. After BDL + vagotomy, rats were fed taurocholate for 1 week in the absence or presence of wortmannin. Caspase involvement was evaluated by measurement of caspase 8, 9 and 3 activities. Proliferation was determined by morphometry and PCNA immunoblots. Changes in PI3K activity were estimated by the expression of the phosphorylated Akt protein. ABAT expression and activity was evaluated by immunoblots and 3H-taurocholate uptake, respectively. Cholangiocyte apoptosis increased whereas proliferation decreased in BDL + vagotomy rats. Taurocholate feeding prevented vagotomy effects on cholangiocyte functions, which were abolished by wortmannin. ABAT expression and activity as well as phosphorylated Akt protein expression was reduced by vagotomy but restored by taurocholate. The activities of caspase 8, 9 and 3 increased in BDL + vagotomy rats but were restored by taurocholate. The protective effect of taurocholate was associated with maintenance of ABAT activity, downregulation of caspase 8, 9 and 3 and activation of PI3K. Bile acids are important in modulating cholangiocyte proliferation in denervated livers.
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