ReferenceID 6484
Vitexin attenuates autoimmune hepatitis in mouse induced by syngeneic liver cytosolic proteins via activation of AMPK/AKT/GSK-3β/Nrf2 pathway
Eur J Pharmacol
Autoimmune hepatitis (AIH) is a chronic progressive liver disease that currently does not have a successful therapeutic option. Vitexin, a bioflavonoid isolated from various medicinal plants, possesses a variety of activ
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Record Fields
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- Reference Id
- 6484
- Evidence Id
- 23074
- Core Evidence Id
- 23074
- Source Reference Id
- 6272
- Herb2 Reference Id
- HBREF007069
- Subject Paper Key
- HBIN048102_34953801
- Pubmed Id
- 34953801
- Doi
- 10.1016/j.ejphar.2021.174720
- Paper Title
- Vitexin attenuates autoimmune hepatitis in mouse induced by syngeneic liver cytosolic proteins via activation of AMPK/AKT/GSK-3β/Nrf2 pathway
- Paper Abstract
- Autoimmune hepatitis (AIH) is a chronic progressive liver disease that currently does not have a successful therapeutic option. Vitexin, a bioflavonoid isolated from various medicinal plants, possesses a variety of activities; however, whether vitexin protects against AIH remains unclear. Therefore, the current study aims to investigate the hepatoprotective effects and mechanism of action of vitexin in both an experimental autoimmune hepatitis (EAH) mouse model and in D-galactosamine/lipopolysaccharide (D-GalN/LPS)-induced hepatocyte injury. Syngeneic liver antigen S100 was used to establish EAH. Vitexin treatment significantly decreased the infiltration of inflammatory and CD4 + T cells in the liver, reduced ALT and AST levels in the serum and attenuated hepatic injury due to oxidative stress. Moreover, vitexin mitigated the upregulation of Bax and cleaved caspase-3 and the downregulation of Bcl-2 in the livers of AIH mice. These regulations were accompanied by not only increased phosphorylation of AMPK, AKT and GSK-3β but also activation of Nrf2. Furthermore, vitexin inhibited apoptosis and the overexpression of inflammatory cytokines in D-GalN/LPS-treated AML12 cells. In addition, vitexin enhanced the phosphorylation of AMPK, AKT and GSK-3β. When AML12 cells were treated with an inhibitor of AMPK/AKT or specific siRNA targeting Nrf2, vitexin did not further induce the activation of Nrf2/HO-1. A molecular docking study confirmed that vitexin could interact with AMPK through hydrogen bonding interactions. In conclusion, vitexin ameliorated hepatic injury in EAH mice through activation of the AMPK/AKT/GSK-3β pathway and upregulation of the Nrf2 gene.
- Journal
- Eur J Pharmacol
- Publish Year
- 2021
- Experiment Subject
- mouse; aml12 cells; d-galn/lps-treated aml12 cells
- Experiment Type
- Animal & Cell Experiment
- Phenotype Related
- Autoimmune Hepatitis; Chronic Progressive Liver Disease
- Paper Title Cn
- Paper Title En
- Vitexin attenuates autoimmune hepatitis in mouse induced by syngeneic liver cytosolic proteins via activation of AMPK/AKT/GSK-3β/Nrf2 pathway
- Bilingual Status
- semi_complete