ReferenceID 5338
Glabridin inhibits liver fibrosis and hepatic stellate cells activation through suppression of inflammation and oxidative stress by activating PPARγ in carbon tetrachloride-treated mice
Int Immunopharmacol
Glabridin is an active ingredient extracted from the root of Glycyrrhiza glabra. Previous studies showed that glabridin had potent hepatoprotective effect, however, the effect of glabridin on liver fibrosis and its poten
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- Reference Id
- 5338
- Evidence Id
- 21928
- Core Evidence Id
- 21928
- Source Reference Id
- 3981
- Herb2 Reference Id
- HBREF004778
- Subject Paper Key
- HBIN027849_36371863
- Pubmed Id
- 36371863
- Doi
- 10.1016/j.intimp.2022.109433
- Paper Title
- Glabridin inhibits liver fibrosis and hepatic stellate cells activation through suppression of inflammation and oxidative stress by activating PPARγ in carbon tetrachloride-treated mice
- Paper Abstract
- Glabridin is an active ingredient extracted from the root of Glycyrrhiza glabra. Previous studies showed that glabridin had potent hepatoprotective effect, however, the effect of glabridin on liver fibrosis and its potential mechanisms remain largely unknown. The present study was aimed to study the effect and potential mechanisms of glabridin on liver fibrosis in carbon tetrachloride (CCl 4 )-treated mouse livers. Glabridin attenuated the liver injury and improved pathological changes in CCl 4 -treated mouse livers. Glabridin suppressed the liver fibrosis in CCl 4 -treated mouse livers, as shown by the decreased collagen deposition, the reduced hydroxyproline level together with the decreased mRNA and protein expression of α-SMA, fibronectin and α1(I)procollagen in mouse livers. Interestingly, glabridin increased the mRNA and protein expression of proliferator-activated receptor gamma (PPARγ) in CCl 4 -treated mouse livers. In addition, both immunohistochemistry and tissue immunofluorescence showed that glabridin upregulated the expression of PPARγ in CCl 4 -treated mouse livers. Glabridin evidently reduced the levels of pro-inflammatory factors and increased the level of anti-inflammatory factor in CCl 4 -treated mouse livers and sera. In addition, Glabridin inhibited the level of MDA and increased the level of GSH as well as the total antioxidant capacity (T-AOC) in CCl 4 -treated mouse livers. In vitro study showed that glabridin reduced the cell viability of PDGF-BB-stimulated JS-1 cells. Noteworthy, glabridin showed no obvious toxicity on normal JS1 cells. Glabridin inhibited the protein expression of α-SMA, fibronectin and α1(I)procollagen, and increased the expression of PPARγ in stimulated JS-1 cells. Furthermore, disruption of PPARγ attenuated the anti-inflammatory and anti-oxidative stress effects of glabridin in stimulated JS-1 cells. Collectively, glabridin inhibited the liver fibrosis and hepatic stellate cells activation by suppressing inflammation and oxidative stress through activation of PPARγ in carbon tetrachloride-treated mice.
- Journal
- Int Immunopharmacol
- Publish Year
- 2022
- Experiment Subject
- mouse; ccl 4; js1 cells; pdgf-bb-stimulated js-1 cells; stimulated js-1 cells
- Experiment Type
- Animal Experiment
- Phenotype Related
- Liver Fibrosis
- Paper Title Cn
- Paper Title En
- Glabridin inhibits liver fibrosis and hepatic stellate cells activation through suppression of inflammation and oxidative stress by activating PPARγ in carbon tetrachloride-treated mice
- Bilingual Status
- semi_complete