Document Type : Original Article

Authors

• Seyedeh Saboura Seyedan ^{1, 2}
• Elham Taheri ³
• Mahdi Amiri ³
• Arezoo Rajabian ^{4, 5}
• Mahmoud Hosseini ^{6, 7}

¹ Applied Biomedical Research Center, Basic Sciences Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran

² Department of Clinical Psychology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.

³ Department of Clinical Psychology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran

⁴ Neuroscience Research Center, Basic Sciences Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran

⁵ Department of Neuroscience, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran

⁶ Psychiatry and Behavioral Sciences Research Center, Mashhad University of Medical Sciences, Mashhad, Iran

⁷ Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran

Abstract

Introduction: Hepatic encephalopathy (HE) is a neuropsychiatric syndrome that develops in the context of acute or chronic hepatic failure. Thiamine (vitamin B1) contributes to neurotransmitter biosynthesis and also exhibits pronounced antioxidant activity. We therefore asked whether vitamin B1 modifies anxiety- and depression-like behavior, as well as markers of cerebral oxidative stress, in rats with thioacetamide (TAA)-induced HE.
Methods: Five groups of rats (n=10 each) were studied: control, TAA, and TAA plus vitamin B1 given orally at 50, 100, or 200 mg/kg. Behavioral assessment comprised elevated plus maze (EPM), open field (OF), rotarod, forced swimming (FS), and sucrose preference tests. Afterward, malondialdehyde (MDA), total thiol, and superoxide dismutase (SOD) activity were measured in brain tissue, and liver injury was gauged by serum alkaline phosphatase (ALKP), aspartate transaminase (AST), and alanine aminotransferase (ALT).
Results: TAA lowered sucrose preference (P<0.001), EPM open-arm time (P<0.001) and entries (P<0.01), time (P<0.001) and travelled distance (P<0.01) in the OF center, rotarod latency to fall (P<0.001), and brain thiol and SOD (P<0.001). It raised FS immobility, EPM closed-arm time (P<0.05), OF peripheral time (P<0.001), the number of rotarod falls (P<0.001), brain MDA (P<0.001), together with the liver enzymes ALT (P<0.01) and ALKP (P<0.001). Treatment with vitamin B1 counteracted these alterations to varying extents. Relative to TAA alone, it enhanced central-zone activity (P<0.01-P<0.001), open-arm exploration (P<0.001), sucrose preference (P<0.05-P<0.001), and rotarod performance (P<0.05-P<0.01), shortened immobility (P<0.05-P<0.001), and normalized brain MDA, thiol, and SOD (P < 0.05 to P < 0.01) as well as ALKP, AST, and ALT (P < 0.01 to P < 0.001).
Conclusions: Vitamin B1 protected against TAA-induced anxiety- and depression-like behavior, motor deficits, and cerebral oxidative stress, supporting its potential as an adjunctive option for the neuropsychiatric complications of HE.
 

Highlights

Mahdi Amiri  (Google Scholar)

Arezoo Rajabian (Google Scholar)

Mahmoud Hosseini (Google Scholar)

 

 

Keywords

• Hepatic encephalopathy
• Thiamine
• Anxiety
• Depressive
• Vitamin B1
• Oxidative stress

Main Subjects

• Neuroscience