Sirtuin‐3 activation by honokiol restores mitochondrial dysfunction in the hippocampus of the hepatic encephalopathy rat model of ammonia neurotoxicity

2021 ◽  
Author(s):  
Anamika ◽  
Surendra K. Trigun
Keyword(s):  
Hepatic Encephalopathy ◽  
Mitochondrial Dysfunction ◽  
Rat Model ◽  
Sirtuin 3 ◽  
Ammonia Neurotoxicity

scholarly journals Neuroprotective Effect of Nortriptyline in Overt Hepatic Encephalopathy Through Attenuation of Mitochondrial Dysfunction

ASN NEURO ◽  
2018 ◽  
Vol 10 ◽  
pp. 175909141881058 ◽  
Author(s):  
Ji Heun Jeong ◽  
Do Kyung Kim ◽  
Nam-Seob Lee ◽  
Young-Gil Jeong ◽  
Ho Won Kim ◽  
...  
Keyword(s):  
Cell Death ◽  
Hepatic Encephalopathy ◽  
Substantia Nigra ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Permeability Transition ◽  
Neuroprotective Effect ◽  
Motor Deficits ◽  
Apoptotic Pathway ◽  
Duct Ligation ◽  
Overt Hepatic Encephalopathy

Hyperammonemia associated with overt hepatic encephalopathy (OHE) causes excitotoxic neuronal death through activation of the cytochrome C (CytC)-mediated mitochondria-dependent apoptotic pathway. We tested the therapeutic effect of nortriptyline (NT), a mitochondrial permeability transition pore (mPTP) blocker that can possibly inhibit mitochondrial CytC efflux to the cytosol on in vivo and in vitro OHE models. After ensuring the generation of OHE rats, established by bile duct ligation (BDL), they were intraperitoneally administered either 20 mg/kg NT (i.e., BDL+NT) or another vehicle (i.e., BDL+VEH) for 14 days. Compared with the control, BDL+VEH showed an increment of motor deficits, cell death, synaptic loss, apoptosis, and mitochondria with aberrant morphology in substantia nigra compacta dopaminergic (DA-ergic) neurons. However, the extent was significantly reversed in BDL+NT. Subsequently, we studied the neuroprotective mechanism of NT using PC-12 cells, a DA-ergic cell line, which exposed glutamate used as an excitotoxin. Compared with the control, the cells exposed to 15 mM glutamate (i.e., GLU) showed incremental cell death, apoptosis, and demise in mitochondrial respiration. Importantly, efflux of CytC from mitochondria to cytosol and the dissipation of mitochondrial membrane potential (△Ψm), an indicator of mPTP opening, were prominent in GLU. However, compared with the GLU, the cells cotreated with 10 μM NT (i.e., GLU+NT) showed a significant reduction in the aforementioned phenomenon. Together, we concluded that NT can be used for OHE therapeutics, mitigating the excitotoxic death of substantia nigra compacta DA-ergic neurons via mPTP-associated mitochondrial dysfunction inhibition.

Acetylcholinesterase activity in an experimental rat model of Type C hepatic encephalopathy

2011 ◽  
Vol 113 (3) ◽  
pp. 358-362 ◽  
Author(s):  
Marta Méndez ◽  
Magdalena Méndez-López ◽  
Laudino López ◽  
María A. Aller ◽  
Jaime Arias ◽  
...  
Keyword(s):  
Hepatic Encephalopathy ◽  
Rat Model ◽  
Acetylcholinesterase Activity ◽  
Experimental Rat Model ◽  
Type C

P: 4 Uncovering Sex-based Differences in a Rat Model of Chronic Liver Disease and Hepatic Encephalopathy

2019 ◽  
Vol 114 (1) ◽  
pp. S2-S2
Author(s):  
Mariana M. Oliveira ◽  
Alexis Monnet-Aimard ◽  
Mélanie Tremblay ◽  
Christopher F. Rose
Keyword(s):  
Liver Disease ◽  
Hepatic Encephalopathy ◽  
Chronic Liver Disease ◽  
Rat Model ◽  
Chronic Liver

scholarly journals Alpha-synuclein-induced mitochondrial dysfunction is mediated via a sirtuin 3-dependent pathway

2020 ◽  
Vol 15 (1) ◽  
Author(s):  
Jae-Hyeon Park ◽  
Jeremy D. Burgess ◽  
Ayman H. Faroqi ◽  
Natasha N. DeMeo ◽  
Fabienne C. Fiesel ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Alpha Synuclein ◽  
Sirtuin 3 ◽  
Dependent Pathway

scholarly journals Impaired Cerebral Mitochondrial Oxidative Phosphorylation Function in a Rat Model of Ventricular Fibrillation and Cardiopulmonary Resuscitation

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Jun Jiang ◽  
Xiangshao Fang ◽  
Yue Fu ◽  
Wen Xu ◽  
Longyuan Jiang ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Ventricular Fibrillation ◽  
Cardiopulmonary Resuscitation ◽  
Oxidative Phosphorylation ◽  
Mitochondrial Dysfunction ◽  
Rat Model ◽  
Mitochondrial Function ◽  
High Energy ◽  
Mitochondrial Morphology ◽  
High Energy Phosphates

Postcardiac arrest brain injury significantly contributes to mortality and morbidity in patients suffering from cardiac arrest (CA). Evidence that shows that mitochondrial dysfunction appears to be a key factor in tissue damage after ischemia/reperfusion is accumulating. However, limited data are available regarding the cerebral mitochondrial dysfunction during CA and cardiopulmonary resuscitation (CPR) and its relationship to the alterations of high-energy phosphate. Here, we sought to identify alterations of mitochondrial morphology and oxidative phosphorylation function as well as high-energy phosphates during CA and CPR in a rat model of ventricular fibrillation (VF). We found that impairment of mitochondrial respiration and partial depletion of adenosine triphosphate (ATP) and phosphocreatine (PCr) developed in the cerebral cortex and hippocampus following a prolonged cardiac arrest. Optimal CPR might ameliorate the deranged phosphorus metabolism and preserve mitochondrial function. No obvious ultrastructural abnormalities of mitochondria have been found during CA. We conclude that CA causes cerebral mitochondrial dysfunction along with decay of high-energy phosphates, which would be mitigated with CPR. This study may broaden our understanding of the pathogenic processes underlying global cerebral ischemic injury and provide a potential therapeutic strategy that aimed at preserving cerebral mitochondrial function during CA.

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