Indole-3-carbinol ameliorated the thioacetamide-induced hepatic encephalopathy in rats

Ramakrishna, Kakarla; Sinku, Sangeetha; Majumdar, Shreyasi; Singh, Neha Atulkumar; Gajendra, T.A; Rani, Asha; Krishnamurthy, Sairam

doi:10.1016/j.tox.2023.153542

Cited by 5 publications

(2 citation statements)

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“…The pathological basis of HE is complex, and its pathogenesis is not yet clear. Beyond the ammonia poisoning theory [ 3 ], inflammatory cytokines [ 4 , 5 , 6 , 7 ], neurosteroids [ 8 , 9 , 10 ], endogenous benzodiazepines [ 11 ], bile acids [ 12 , 13 ], and manganese [ 8 ] may participate in the occurrence of HE. In recent years, many researchers have found that the influence of ammonia on neurotransmitters plays an important role in the pathogenesis of HE [ 14 , 15 ].…”

Section: Introductionmentioning

confidence: 99%

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The Mechanism of Hepatic Encephalopathy Induced by Thioacetamide Based on Metabolomics and Proteomics: A Preliminary Study

Guo,

Wang,

Huang

et al. 2023

IJMS

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Hepatic encephalopathy (HE) is a central nervous system dysfunction syndrome caused by acute and chronic liver failure or various portal systemic shunt disorders. HE arises from metabolic disorder and excludes other known types of encephalopathy. HE is a major cause of death in people with liver disease. Early diagnosis and timely treatment are key to improving HE prognosis. Herein, we established a model of HE and performed metabolomics to identify 50 significantly differential metabolites between the HE group and control group. The main metabolic pathways associated with these differential metabolites were the purine metabolism, pyrimidine metabolism, aminoacyl tRNA biosynthesis, and glucose metabolism. Through proteomics analysis, we identified 226 significantly differential proteins (52 up-regulated and 174 down-regulated). The main (Kyoto Encyclopedia of Genes and Genomes) enrichment pathways were the Staphylococcus aureus infection, vitamin digestion and absorption, and complement and coagulation cascades. Through the conjoint analysis of proteomics and metabolomics, the differentially present proteins and metabolites were found to be involved in vitamin digestion and absorption, and ferroptosis pathways. In HE, malondialdehyde was significantly elevated, but glutathione was significantly diminished, and the redox balance was destroyed, thus leading to changes in proteins’ levels associated with the ferroptosis pathway. In conclusion, this study preliminarily explored the molecular and metabolic mechanisms underlying HE.

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Section: Introductionmentioning

confidence: 99%

“…The pathological basis of HE is complex, and its pathogenesis is not yet clear. Beyond the ammonia poisoning theory [3], inflammatory cytokines [4][5][6][7], neurosteroids [8][9][10],…”

Section: Introductionmentioning

confidence: 99%