ReferenceID 5280
Galangin mitigates iron overload-triggered liver injury: Up-regulation of PPARγ and Nrf2 signaling, and abrogation of the inflammatory responses
Life Sci
AIM: Hepatotoxicity is a critical consequence of the iron overload conditions such as hemochromatosis and blood transfusion-requiring anemia. Iron induces hepatotoxicity largely through disruption of cellular redox homeo
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- Reference Id
- 5280
- Evidence Id
- 21870
- Core Evidence Id
- 21870
- Source Reference Id
- 3823
- Herb2 Reference Id
- HBREF004620
- Subject Paper Key
- HBIN027003_34329667
- Pubmed Id
- 34329667
- Doi
- 10.1016/j.lfs.2021.119856
- Paper Title
- Galangin mitigates iron overload-triggered liver injury: Up-regulation of PPARγ and Nrf2 signaling, and abrogation of the inflammatory responses
- Paper Abstract
- AIM: Hepatotoxicity is a critical consequence of the iron overload conditions such as hemochromatosis and blood transfusion-requiring anemia. Iron induces hepatotoxicity largely through disruption of cellular redox homeostasis and induction of inflammatory responses. The present work explored the hepatoprotective activity of the bio-active flavone galangin against iron-evoked hepatotoxicity. MAIN METHODS: Iron overload model was established in male Wistar rats via intraperitoneal injection of 150 mg/kg iron-dextran subdivided over a ten-day experimental period. Galangin was administered in a daily oral dose of 15 mg/kg throughout the experimental period. Blood and liver tissue samples were collected on day eleven and subjected to biochemical and molecular investigations. KEY FINDINGS: Galangin significantly reduced liver iron content and serum ferritin level, and alleviated the iron-evoked oxidative stress. It enhanced the liver cell integrity as reflected by decreased serum activity of the liver enzymes. Mechanistically, galangin up-regulated the redox-regulating transcription factor Nrf2 and its responsive proteins HO-1 and NQO1. Interestingly, galangin up-regulated the antioxidant and anti-inflammatory protein PPARgamma and serum hepcidin levels under the iron overload conditions. Equally important, it diminished the nuclear shift of the inflammatory transcription factor NF-kappaB p65 and down-regulated the levels of the pro-inflammatory cytokines TNF-alpha and IL-1beta. SIGNIFICANCE: The results of the present study highlight the mitigating activity of galangin against iron-induced hepatotoxicity. The study accentuated targeting of Nrf2, PPARgamma, and NF-kappaB signaling as potential contributing mechanisms. While clinical studies are still required, the current study supports the possible implementation of galangin in controlling iron overload-associated hepatotoxicity.
- Journal
- Life Sci
- Publish Year
- 2021
- Experiment Subject
- rat
- Experiment Type
- Animal Experiment
- Phenotype Related
- Iron Overload Conditions; Iron Overload-associated Hepatotoxicity; Hemochromatosis; Anemia; Hepatotoxicity
- Paper Title Cn
- Paper Title En
- Galangin mitigates iron overload-triggered liver injury: Up-regulation of PPARγ and Nrf2 signaling, and abrogation of the inflammatory responses
- Bilingual Status
- semi_complete