PUBLICATION
Lupeol ameliorates LPS/D-GalN induced acute hepatic damage by suppressing inflammation and oxidative stress through TGFβ1-Nrf2 signal pathway
- Authors
- Huang, S., Mo, C., Zeng, T., Lai, Y., Zhou, C., Xie, S., Chen, L., Wang, Y., Chen, Y., Huang, S., Gao, L., Lv, Z.
- ID
- ZDB-PUB-210313-1
- Date
- 2021
- Source
- Aging 13(5): 6592-6605 (Journal)
- Registered Authors
- Keywords
- Nrf2, TGFβ1, acute liver injury, inflammation, lupeol
- MeSH Terms
-
- Animals
- Anti-Inflammatory Agents/pharmacology*
- Chemical and Drug Induced Liver Injury/prevention & control*
- Disease Models, Animal
- Down-Regulation
- Galactosamine/toxicity
- Inflammation/prevention & control
- Lipopolysaccharides/toxicity
- Mice, Inbred C57BL
- NF-E2-Related Factor 2/metabolism*
- Oxidative Stress/drug effects
- Pentacyclic Triterpenes/pharmacology*
- Transforming Growth Factor beta1/metabolism*
- Up-Regulation
- Zebrafish
- PubMed
- 33707345 Full text @ Aging (Albany NY)
Citation
Huang, S., Mo, C., Zeng, T., Lai, Y., Zhou, C., Xie, S., Chen, L., Wang, Y., Chen, Y., Huang, S., Gao, L., Lv, Z. (2021) Lupeol ameliorates LPS/D-GalN induced acute hepatic damage by suppressing inflammation and oxidative stress through TGFβ1-Nrf2 signal pathway. Aging. 13(5):6592-6605.
Abstract
Acute hepatic damage is a severe condition characterized by inflammation and oxidative stress, which is a serious threat to people's life and health. But there are few effective treatments for acute liver injury. Therefore, safe and effective therapeutic approaches for preventing acute liver damage are urgently needed. Lupeol is a natural compound, which has significant antioxidant and anti-inflammatory properties in liver disease. However, the protective mechanism of lupeol against acute liver injury remains unclear. Here, zebrafish and mutant mice were utilized to investigate the protective effects of lupeol against lipopolysaccharide (LPS)/ D-galactosamine(D-GalN) -induced liver injury and the underlying mechanisms. We found that pretreatment with lupeol attenuated the LPS/D-GalN-induced liver injury by decreasing the infiltration of inflammatory cells and reducing pro-inflammatory cytokines. We also demonstrated that lupeol could protect injured liver from oxidative stress by downregulating the expression of TGFβ1 and upregulating Nrf2. Notably, our experimental results provided the support that lupeol effectively protected against LPS/D-GalN-induced acute liver injury via suppression of inflammation response and oxidative stress, which were largely dependent on the upregulation of the Nrf2 pathway via downregulating TGFβ1.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping