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Decreased brain noradrenaline in minimal hepatic encephalopathy is associated with cognitive impairment in rats
Xuhong Yang1, Wenxiao Liu1, Pei Dang2
1School of Clinical Medicine, Ningxia Medical University, Yinchuan 750004, China.
Background And Aims:
Minimal hepatic encephalopathy (MHE) is a common neuropsychiatric complication in patients with cirrhosis. Alterations in monoamine neurotransmitters have been associated with the pathogenesis of MHE. We investigated the levels of hippocampal noradrenergic neurotransmitter in a rat model of thioacetamide-induced chronic liver failure-related MHE, and their role in cognitive impairment.
Materials:
18 male Sprague-Dawley (SD) rats were equally divided in MHE and control groups. A rat model of MHE was established by intraperitoneal injection of thioacetamide (TAA) for 12 weeks. Cognitive function was assessed using the Morris water maze (MWM) test and locomotor activity and exploratory behavior assessed with open field test. The concentration of hippocampal noradrenaline (NE) was detected by ELISA, and the magnetic susceptibility value in the hippocampus was detected by quantitative susceptibility mapping. Hippocampal iron content was quantified by Prussian blue staining.
Results:
MHE rats performed significantly poorer than their control counterparts in the MWM test, as seen by decreased number of platform crossings and time in the target quadrant, and increased path length to reach the target zone (P < 0.05 for all parameters). In the open field test, the MHE group exhibited lower locomotor activity and exploratory behavior than the control group (P < 0.05 for all parameters). We detected pronounced iron staining in the hippocampus of MHE rats, whereas no iron-stained particles were found in control rats. We observed an imbalance of inflammatory (increased pro- and decreased anti-) cytokines in the hippocampus of MHE rats. Further analysis of the data showed that the level of hippocampal noradrenaline in MHE rats was significantly lower than that of control rats (P < 0.05). We observed a correlation between the level of inflammatory cytokine and noradrenaline land susceptibility value in the rat hippocampus of the MHE group.
Conclusion:
Our results suggest that MHE associated with TAA-induced chronic liver failure is associated with alterations in noradrenergic neurotransmission. We propose that iron imbalance in the brain might lead to reduction in the levels of noradrenaline, and cognitive impairment.
Insights
Minimal hepatic encephalopathy (MHE) in rats with liver failure showed reduced hippocampal noradrenaline levels and impaired cognition. Iron accumulation in the brain may cause these MHE-related changes.
Area of Science:
- Neuroscience
- Hepatology
- Biochemistry
Background:
- Minimal hepatic encephalopathy (MHE) is a common neuropsychiatric complication in cirrhosis patients.
- Alterations in monoamine neurotransmitters are implicated in MHE pathogenesis.
- Investigating hippocampal noradrenergic neurotransmitter alterations in MHE is crucial.
Purpose of the Study:
- To investigate hippocampal noradrenergic neurotransmitter levels in a rat model of thioacetamide-induced chronic liver failure-related MHE.
- To explore the role of these neurotransmitters in cognitive impairment associated with MHE.
- To examine the relationship between iron accumulation, inflammation, and noradrenergic changes in MHE.
Main Methods:
- Established a thioacetamide (TAA)-induced rat model of chronic liver failure-related MHE over 12 weeks.
- Assessed cognitive function using the Morris water maze (MWM) and exploratory behavior via open field test.
- Quantified hippocampal noradrenaline (NE) levels (ELISA), iron content (Prussian blue staining), and magnetic susceptibility.
Main Results:
- MHE rats exhibited significant cognitive deficits and reduced locomotor activity compared to controls.
- Pronounced hippocampal iron accumulation was observed in MHE rats, absent in controls.
- Significantly lower hippocampal noradrenaline levels and altered inflammatory cytokine profiles were found in MHE rats.
Conclusions:
- Thioacetamide-induced MHE in rats is linked to altered noradrenergic neurotransmission.
- Brain iron imbalance may contribute to reduced noradrenaline levels and cognitive impairment in MHE.
- Findings suggest a potential mechanism involving iron dysregulation in MHE pathogenesis.
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