ReferenceID 5671
Mangiferin Attenuates LPS/D-GalN-Induced Acute Liver Injury by Promoting HO-1 in Kupffer Cells
Front Immunol
Acute liver injury and its terminal phase, hepatic failure, trigger a series of complications, including hepatic encephalopathy, systematic inflammatory response syndrome, and multiorgan failure, with relatively high mor
Relationship Network
Interactive first-hop connections across herbs, ingredients, formulas, targets, diseases, symptoms, syndromes, evidence, and monographs.
Click a node to open it in a new tab
Ingredient: 1Reference: 1Links: 1
Arranging relationship network...
Record Fields
Scalar fields from the final reference record.
- Reference Id
- 5671
- Evidence Id
- 22261
- Core Evidence Id
- 22261
- Source Reference Id
- 4581
- Herb2 Reference Id
- HBREF005378
- Subject Paper Key
- HBIN034394_32158448
- Pubmed Id
- 32158448
- Doi
- 10.3389/fimmu.2020.00285
- Paper Title
- Mangiferin Attenuates LPS/D-GalN-Induced Acute Liver Injury by Promoting HO-1 in Kupffer Cells
- Paper Abstract
- Acute liver injury and its terminal phase, hepatic failure, trigger a series of complications, including hepatic encephalopathy, systematic inflammatory response syndrome, and multiorgan failure, with relatively high morbidity and mortality. Liver transplantation is the ultimate intervention, but the shortage of donor organs has limited clinical success. Mangiferin (MF), a xanthone glucoside, has been reported to have excellent anti-inflammatory efficacy. Here, a lipopolysaccharide (LPS)/D-galactosamine (D-GalN)-induced acute liver injury mouse model was established to investigate the protective role of MF and the underlying mechanisms of action. Pretreatment with MF improved survival, decreased serum aminotransferase activities, and inhibited hepatic TNF-alpha production in LPS/D-GalN-challenged mice. Through Kupffer cell (KC) deletion by GdCl3 and KC adoptive transfer, KCs were confirmed to be involved in these beneficial effects of MF. MF reduced LPS-mediated TNF-alpha production via the suppression of the TLR4/NF-kappaB signaling pathway in vitro. MF promoted HO-1 expression, but the knockdown of HO-1 prevented TNF-alpha inhibition, suggesting that the damage-resistance effects of HO-1 occurred via the suppression of TNF-alpha synthesis. When HO-1-silenced KCs were transferred to the liver with KC deletion, the protective effect of MF against LPS/D-GalN-induced acute liver injury was reduced, illustrating the role of KC-derived HO-1 in the anti-injury effects of MF. Collectively, MF attenuated acute liver injury induced by LPS/D-GalN via the inhibition of TNF-alpha production by promoting KCs to upregulate HO-1 expression.
- Journal
- Front Immunol
- Publish Year
- 2020
- Experiment Subject
- mouse; ho-1-silenced kcs
- Experiment Type
- Animal & Cell Experiment
- Phenotype Related
- Hepatic Encephalopathy; Hepatic Failure; Acute Liver Injury; Inflammatory Response Syndrome; Multiorgan Failure
- Paper Title Cn
- Paper Title En
- Mangiferin Attenuates LPS/D-GalN-Induced Acute Liver Injury by Promoting HO-1 in Kupffer Cells
- Bilingual Status
- semi_complete