Protective effect of dioscin against thioacetamide-induced acute liver injury via FXR/AMPK signaling pathway in vivo. |
Authors: |
Zheng, Lingli Yin, Lianhong Xu, Lina Qi, Yan Li, Hua Xu, Youwei Han, Xu Liu, Kexin Peng, Jinyong
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Citation: |
Zheng L, etal., Biomed Pharmacother. 2018 Jan;97:481-488. doi: 10.1016/j.biopha.2017.10.153. Epub 2017 Nov 6. |
RGD ID: |
15090820 |
Pubmed: |
(View Article at PubMed) PMID:29091898 |
DOI: |
Full-text: DOI:10.1016/j.biopha.2017.10.153 |
Our previous works showed that dioscin, a natural product, could protect liver from acute liver damages induced by dimethylnitrosamine, ethanol, carbon tetrachloride and acetaminophen. However, the effect of dioscin on thioacetamide (TAA)-induced acute liver injury still remained unknown. The purpose of this study was to investigate whether dioscin confers a protective effect against TAA-induced acute liver injury in rats and mice. The results showed that dioscin decreased the serum levels of ALT, AST, and rehabilitated histopathological changes compared with the model groups. In addition, dioscin obviously increased the levels of GSH, GSH-Px, SOD, and significantly reduced MDA levels compared with the model groups. Mechanistic study showed that dioscin significantly up-regulated the expression levels of FXR, p-AMPKα, and then increased the expression levels of Nrf2, HO-1, NQO-1, GCLM and GST. Furthermore, dioscin obviously down-regulated the expression levels of NF-κB (p65), ICAM-1, HMGB1, COX-2, TNF-α, IL-1β and IL-6. Taken together, dioscin showed protective effect against TAA-induced acute liver injuries in rats and mice and the effects might be obtained through inhibiting oxidative stress and inflammation via FXR/AMPK signal pathway. These findings provided a new insight on the role of doscin in the treatment of acute liver injury.
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Annotation
Gene-Chemical Interaction Annotations
Gene Ontology Annotations
Molecular Pathway Annotations
Objects Annotated
Genes (Rattus norvegicus) |
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Hmgb1 (high mobility group box 1) | Hmox1 (heme oxygenase 1) | Icam1 (intercellular adhesion molecule 1) | Il1b (interleukin 1 beta) | Il6 (interleukin 6) |
| Nfe2l2 (nuclear factor, erythroid 2-like 2) | Nfkb1 (nuclear factor kappa B subunit 1) | Nqo1 (NAD(P)H quinone dehydrogenase 1) | Nr1h4 (nuclear receptor subfamily 1, group H, member 4) | Prkaa1 (protein kinase AMP-activated catalytic subunit alpha 1) |
| Ptgs2 (prostaglandin-endoperoxide synthase 2) | Tnf (tumor necrosis factor) |
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Genes (Mus musculus) |
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Hmgb1 (high mobility group box 1) | Hmox1 (heme oxygenase 1) | Icam1 (intercellular adhesion molecule 1) | Il1b (interleukin 1 beta) | Il6 (interleukin 6) |
| Nfe2l2 (nuclear factor, erythroid derived 2, like 2) | Nfkb1 (nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105) | Nqo1 (NAD(P)H dehydrogenase, quinone 1) | Nr1h4 (nuclear receptor subfamily 1, group H, member 4) | Prkaa1 (protein kinase, AMP-activated, alpha 1 catalytic subunit) |
| Ptgs2 (prostaglandin-endoperoxide synthase 2) | Tnf (tumor necrosis factor) |
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Genes (Homo sapiens) |
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HMGB1 (high mobility group box 1) | HMOX1 (heme oxygenase 1) | ICAM1 (intercellular adhesion molecule 1) | IL1B (interleukin 1 beta) | IL6 (interleukin 6) |
| NFE2L2 (nuclear factor, erythroid 2 like 2) | NFKB1 (nuclear factor kappa B subunit 1) | NQO1 (NAD(P)H quinone dehydrogenase 1) | NR1H4 (nuclear receptor subfamily 1 group H member 4) | PRKAA1 (protein kinase AMP-activated catalytic subunit alpha 1) |
| PTGS2 (prostaglandin-endoperoxide synthase 2) | TNF (tumor necrosis factor) |
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Additional Information
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