ArticleMolecular and cellular biochemistry2011
Mitochondrial dysfunction as a mediator of hippocampal apoptosis in a model of hepatic encephalopathy.
Article in Molecular and cellular biochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 32 citations in OpenAlex.
- Involvement of SIRT3 downstream targets ANT1, VDAC, CYPD, and Drp1 in a rat model of hepatic encephalopathy: Therapeutic role of thymoquinone.Iranian journal of basic medical sciences · 2026Article
- Gallic acid alleviates hippocampus and cerebellum injuries in a rat model of hepatic encephalopathy.Scientific reports · 2025Article
- Protective role of VEGF/VEGFR2 signaling against high fatality associated with hepatic encephalopathy via sustaining mitochondrial bioenergetics functions.Journal of biomedical science · 2022Article
- Curcumin prevents cognitive deficits in the bile duct ligated rats.Psychopharmacology · 2020Article
- The Changes of Mitochondria in Substantia Nigra and Anterior Cerebral Cortex of Hepatic Encephalopathy Induced by Thioacetamide.Anatomical record (Hoboken, N.J. : 2007) · 2019Article
- Nicotine Modulates Mitochondrial Dynamics in Hippocampal Neurons.Molecular neurobiology · 2018Article
- Hepatic encephalopathy changes mitochondrial dynamics and autophagy in the substantia nigra.Metabolic brain disease · 2018Article
- Mitochondrial dysfunctions contribute to energy deficits in rodent model of hepatic encephalopathy.Metabolic brain disease · 2018Article
- Nitrosative Stress-Induced Disruption of Baroreflex Neural Circuits in a Rat Model of Hepatic Encephalopathy: A DTI Study.Scientific reports · 2017Article
- Cytokine levels contribute to the pathogenesis of minimal hepatic encephalopathy in patients with hepatocellular carcinoma via STAT3 activation.Scientific reports · 2016Article
- Inhibition of G protein-coupled receptor 81 (GPR81) protects against ischemic brain injury.CNS neuroscience & therapeutics · 2015Article
- Oxygen metabolism in human placenta mitochondria.Journal of bioenergetics and biomembranes · 2014Article
- Current pathogenetic aspects of hepatic encephalopathy and noncirrhotic hyperammonemic encephalopathy.World journal of gastroenterology · 2013Review
- Hepatic encephalopathy: An approach to its multiple pathophysiological features.World journal of hepatology · 2012Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, we describe the presence of apoptosis, associated with a mitochondrial dysfunction in the hippocampus of animals in an experimental model defined as minimal hepatic encephalopathy (MHE). This experimental model was studied after 10 days of induced portal vein calibrated stricture, leading to portal hypertension and to a moderate hyperammonemia, without the presence of other evident central nervous system changes. The molecular mechanisms here proposed indicate the presence of apoptotic intrinsic pathways that point to hippocampal mitochondria as an important mediator of apoptosis in this experimental model. In this model of MHE, the presence of DNA fragmentation is documented by 2.3-times increased number of TUNEL-positive cells. These findings together with a higher ratio of the Bcl-2 family members Bax/Bcl-xL in the outer mitochondrial membrane of the MHE animals together with 11% of cytochrome c release indicate the presence of apoptosis in this experimental model. A detailed analysis of the hippocampal mitochondrial physiology was performed after mitochondrial isolation. The determination of the respiratory rate in the presence of malate plus glutamate and ADP showed a 45% decrease in respiratory control in MHE animals as compared with the sham group. A marked decrease of cytochrome oxidase (complex IV of the electron transport chain) was also observed, showing 46% less activity in hippocampal mitochondria from MHE animals. In addition, mitochondria from these animals showed less ability to maintain membrane potential (ΔΨ (m)) which was 13% lower than the sham group. Light scattering experiments showed that mitochondria from MHE animals were more sensitive to swell in the presence of increased calcium concentrations as compared with the sham group. In addition, in vitro studies performed in mitochondria from sham animals showed that mitochondrial permeability transition (MPT) could be a mitochondrial mediator of the apoptotic signaling in the presence of NH(4) (+) and calcium.
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