scholarly journals Bacopa monnieriExtract (CDRI-08) Modulates the NMDA Receptor Subunits and nNOS-Apoptosis Axis in Cerebellum of Hepatic Encephalopathy Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Papia Mondal ◽  
Surendra Kumar Trigun
Keyword(s):  
Nitric Oxide ◽  
Hepatic Encephalopathy ◽  
Liver Failure ◽  
Chronic Liver ◽  
Chronic Liver Failure ◽  
Apoptosis Pathway ◽  
Nitric Oxide Level ◽  
Nmdar Activation ◽  
Oxide Synthase ◽  
The Brain

Hepatic encephalopathy (HE), characterized by impaired cerebellar functions during chronic liver failure (CLF), involves N-methyl-D-aspartate receptor (NMDAR) overactivation in the brain cells.Bacopa monnieri(BM) extract is a known neuroprotectant. The present paper evaluates whether BM extract is able to modulate the two NMDAR subunits (NR2A and NR2B) and its downstream mediators in cerebellum of rats with chronic liver failure (CLF), induced by administration of 50 mg/kg bw thioacetamide (TAA) i.p. for 14 days, and in the TAA group rats orally treated with 200 mg/kg bw BM extract from days 8 to 14. NR2A is known to impart neuroprotection and that of NR2B induces neuronal death during NMDAR activation. Neuronal nitric oxide synthase- (nNOS-) apoptosis pathway is known to mediate NMDAR led excitotoxicity. The level of NR2A was found to be significantly reduced with a concomitant increase of NR2B in cerebellum of the CLF rats. This was consistent with significantly enhanced nNOS expression, nitric oxide level, and reduced Bcl2/Bax ratio. Moreover, treatment with BM extract reversed the NR2A/NR2B ratio and also normalized the levels of nNOS-apoptotic factors in cerebellum of those rats. The findings suggest modulation of NR2A and NR2B expression by BM extract to prevent neurochemical alterations associated with HE.

scholarly journals Hepatic Encephalopathy-Associated Cerebral Vasculopathy in Acute-on-Chronic Liver Failure: Alterations on Endothelial Factor Release and Influence on Cerebrovascular Function

2020 ◽  
Vol 11 ◽  
Author(s):  
Laura Caracuel ◽  
Esther Sastre ◽  
María Callejo ◽  
Raquel Rodrigues-Díez ◽  
Ana B. García-Redondo ◽  
...  
Keyword(s):  
Hepatic Encephalopathy ◽  
Liver Failure ◽  
Cerebral Arteries ◽  
Chronic Liver ◽  
Chronic Liver Failure ◽  
Cerebrovascular Function ◽  
Liver Decompensation ◽  
Middle Cerebral Arteries ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

The acute-on-chronic liver failure (ACLF) is a syndrome characterized by liver decompensation, hepatic encephalopathy (HE) and high mortality. We aimed to determine the mechanisms implicated in the development of HE-associated cerebral vasculopathy in a microsurgical liver cholestasis (MHC) model of ACLF. Microsurgical liver cholestasis was induced by ligating and extracting the common bile duct and four bile ducts. Sham-operated and MHC rats were maintained for eight postoperative weeks Bradykinin-induced vasodilation was greater in middle cerebral arteries from MHC rats. Both Nω-Nitro-L-arginine methyl ester and indomethacin diminished bradykinin-induced vasodilation largely in arteries from MHC rats. Nitrite and prostaglandin (PG) F1α releases were increased, whereas thromboxane (TX) B2 was not modified in arteries from MHC. Expressions of endothelial nitric oxide synthase (eNOS), inducible NOS, and cyclooxygenase (COX) 2 were augmented, and neuronal NOS (nNOS), COX-1, PGI2 synthase, and TXA2S were unmodified. Phosphorylation was augmented for eNOS and unmodified for nNOS. Altogether, these endothelial alterations might collaborate to increase brain blood flow in HE.

scholarly journals Glutamate-induced activation of nitric oxide synthase is impaired in cerebral cortexin vivoin rats with chronic liver failure

2007 ◽  
Vol 102 (1) ◽  
pp. 51-64 ◽  
Author(s):  
Regina Rodrigo ◽  
Slaven Erceg ◽  
Jesus Rodriguez-Diaz ◽  
Javier Saez-Valero ◽  
Blanca Piedrafita ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Liver Failure ◽  
Chronic Liver ◽  
Chronic Liver Failure ◽  
Oxide Synthase

Cirrhosis and acute on chronic liver failure: is ammonia a predictor of hepatic encephalopathy and mortality?

2017 ◽  
Vol 66 (1) ◽  
pp. S559
Author(s):  
M. Sheikh ◽  
N. Arias ◽  
K. Thomsen ◽  
R. Gallego-Durán ◽  
B. Agarwal ◽  
...  
Keyword(s):  
Hepatic Encephalopathy ◽  
Liver Failure ◽  
Chronic Liver ◽  
Chronic Liver Failure

Liver failure

2020 ◽  
pp. 3089-3100
Author(s):  
Jane Macnaughtan ◽  
Rajiv Jalan
Keyword(s):  
Liver Transplantation ◽  
Liver Disease ◽  
Hepatic Encephalopathy ◽  
Liver Injury ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Organ Failure ◽  
Clinical Manifestations ◽  
Chronic Liver ◽  
Chronic Liver Failure

Liver failure occurs when loss of hepatic parenchymal function exceeds the capacity of hepatocytes to regenerate or repair liver injury. Acute liver failure is characterized by jaundice and prolongation of the prothrombin time in the context of recent acute liver injury, with hepatic encephalopathy occurring within 8 weeks of the first onset of liver disease. Acute-on-chronic liver failure is characterized by hepatic and/or extrahepatic organ failure in patients with cirrhosis associated with an identified or unidentified precipitating event. The commonest causes of acute liver failure are acute viral hepatitis and drugs. Acute-on-chronic liver failure is most commonly precipitated by infection, alcohol abuse, and superimposed viral infection. The main clinical manifestations are hepatic encephalopathy, coagulopathy, jaundice, renal dysfunction, and haemodynamic instability. Infection and systemic inflammation contribute to pathogenesis and critically contribute to prognosis. Specific therapy for the underlying liver disease is administered when available, but this is not possible for most causes of liver failure. Treatment is predominantly supportive, with particular emphasis on (1) correction or removal of precipitating factors; (2) if encephalopathy is present, using phosphate enemata, nonhydrolysed disaccharide laxatives, and/or rifaximin; (3) early detection and prompt treatment of complications such as hypoglycaemia, hypokalaemia, cerebral oedema, infection, and bleeding. The onset of organ failure should prompt discussion with a liver transplantation centre. The mortality of acute liver failure (without liver transplantation) is about 40%. Patients with acute liver failure who do not develop encephalopathy can be expected to recover completely. Those who recover from an episode of acute-on-chronic liver failure should be considered for liver transplantation because otherwise their subsequent mortality remains high.

scholarly journals The brain in acute on chronic liver failure

2014 ◽  
Vol 29 (4) ◽  
pp. 965-973 ◽  
Author(s):  
Gavin Wright ◽  
Yalda Sharifi ◽  
Maria Jover-Cobos ◽  
Rajiv Jalan
Keyword(s):  
Liver Failure ◽  
Chronic Liver ◽  
Chronic Liver Failure ◽  
The Brain

Acute-on-chronic liver failure: the brain

2011 ◽  
Vol 17 (2) ◽  
pp. 177-183 ◽  
Author(s):  
Rita García-Martínez ◽  
Juan Córdoba
Keyword(s):  
Liver Failure ◽  
Chronic Liver ◽  
Chronic Liver Failure ◽  
The Brain

scholarly journals Hepatoprotective Effect of Yiqijianpi Formula (YQJPF) on Liver Failure Through Modulation of Hypoxic and Apoptosis Pathways

2020 ◽  
Author(s):  
Li Tang ◽  
Feixia Wang ◽  
Lingyan Xiao ◽  
Min Shen ◽  
Siwei Xia ◽  
...  
Keyword(s):  
Liver Injury ◽  
Liver Failure ◽  
Signaling Pathways ◽  
Tunel Assay ◽  
Chronic Liver ◽  
Active Components ◽  
Chronic Liver Failure ◽  
Apoptosis Pathway ◽  
L02 Cells

Abstract BackgroundAcute-on-chronic liver failure (ACLF) is a severe complication of cirrhosis, which seriously endanger human life and health. Yiqijianpi decoction (YQJPF) is a Traditional Chinese Medicine (TCM) formula that has been widely used in the treatment of liver failure with significant effect. The purpose of this study was to investigate the active components and mechanism to ameliorate acute on chronic liver failure(ACLF).MethodsLPS combined with D-Gal was used to establish the rat model of ACLF, pathological examination was detected by H&E staining, liver function test was assayed by ELISA. LPS was used to induce hepatocytes injury in vitro. Cell proliferation assay, TUNEL assay were used in human hepatic L02 cells. The active components and putative targets of YQJPF were predicted by network pharmacology approach and GEO analysis. Functional and pathway enrichment analysis were presented by using String, Cytoscape and Metascape. Further, experimental validation was done to verify the effect of YQJPF on PI3K/AKT-HIF-1ɑ and apoptosis-related signaling pathways by using Immunohistochemistry and Western blotting.ResultsAfter being treated with YQJPF, the rat liver injury and fibrosis were alleviated, and Cell Counting Kit-8 assay, TUNEL assay indicated YQJPF also inhibited the apoptosis in hepatic L02 cells. Through network pharmacologic analysis, 135 active components in YQJPF decoction, 573 known therapeutic targets and 2940 liver failure-related human genes were identified. 163 gene symbols maybe the key for liver failure treatment by YQJPF decoction. VEGF-A was hub gene in PPI network. The KEGG pathway and GO enrichment analyses indicated that the PI3K/AKT, HIF-1 signaling pathways were the prominently enriched signaling pathways. In vivo, YQJPF upregulated the expression of PI3K/AKT-HIF1-ɑ and VEGF-A. Moreover apoptosis pathway were verified by up-regulating Bcl2 expression and down-regulating Bax expression in vivo and in vitro.ConclusionYQJPF is beneficial for alleviating liver failure, may regulate hypoxic liver injury through PI3K/AKT-HIF1α dependent apoptosis pathway.

Hepatic disorders

2011 ◽  
Author(s):  
Carl Waldmann ◽  
Neil Soni ◽  
Andrew Rhodes
Keyword(s):  
Hepatic Encephalopathy ◽  
Liver Function ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Serum Bilirubin ◽  
Liver Function Tests ◽  
Abnormal Liver Function ◽  
Chronic Liver ◽  
Bile Pigments ◽  
Chronic Liver Failure

Jaundice 348Acute liver failure 350Hepatic encephalopathy 352Chronic liver failure 354Abnormal liver function tests 356Jaundice (icterus) is the accumulation of bile pigments in serum and tissues including sclerae and skin. Jaundice is usually clinically detectable once serum bilirubin exceeds 50...

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