Abstract
Introduction: Hepatic encephalopathy (HE) is a brain disorder with impairment of cognitive and motor functions caused by liver failure. The aim of this study was to evaluate changes in nociception threshold as well as gene expression of mu-opioid receptor 1 (MOR1) in rat liver after induction of HE. Materials and Methods: The male rats (280-320 g) were randomly divided into three groups of control (non-operated), sham (operated without common bile duct ligation) and a group with a common bile duct ligation (BDL) as an experimental model of HE. Changes in nociception threshold were assessed on day 21 of BDL, using a hotplate test. On day 21 of BDL, rats were weighed, sacrificed and total liver tissue was dissected and weighed, then percentage of liver to body weight was measured. In addition, blood samples were collected for biochemical analysis of serum, and a piece of the liver of each rat was dissected for evaluating the MOR1 gene expression. Results: The results showed that nociception threshold, percentage of liver to body weights, and serum levels of total bilirubin were significantly increased in the HE model group compared to the sham group (P<0.001). Blood urea nitrogen was also increased in this group compared to the sham group (P<0.01). The results also revealed that the MOR1 gene expression at mRNA levels in liver of rats with BDL was significantly decreased compared to the sham group ( P<0.001). Conclusion: Our data indicate that chronic liver failure modulates the MOR1 gene expression in liver. In addition, changes in nociception threshold may confirm a slowness of sensory processing in HE.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
