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Published on: July 19, 2024
Honokiol Mitigates Metabolic-Associated Fatty Liver Disease by Regulating Nrf2 and RIPK3 Signaling Pathways
Wen Cao1, Zengdian Chen1, Chenhui Lin1
1Department of Gastroenterology, Fuzhou Second General Hospital, Fuzhou, Fujian Province, China.
Background/Aims:
Metabolic-associated fatty liver disease (MAFLD) is a common cause of chronic liver disease worldwide. However, there is currently no recognized effective drugs for treating it.
Materials And Methods:
In this study, we investigated the efficacy of Honokiol (HNK) in vitro for mitigating MAFLD. Then, 0.4 mM palmitic acid (PA) and LO2 cells were used to establish the MAFLD model. The protective effect of HNK on MAFLD was confirmed by Oil Red O staining and cell counting kit (CCK-8) assay in LO2 cell line. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were carried out to analyze the regulatory role of HNK on Nrf2 and RIPK3 signaling pathways. The effect of HNK and its downstream signaling pathways on oxidative stress were verified by the detection of reactive oxygen species (ROS), malondialdehyde (MDA), catalase (CAT), and superoxide dismutase (SOD). The concentration of IL-1β, IL-6L, and TNF-α was assessed by enzyme-linked immunosorbent assay (ELISA).
Results:
The middle concentration of HNK (50 μmol/L) was selected as the best option for inhibiting lipidosis and oxidative stress in MAFLD models. Honokiol mitigates MAFLD via activation of nuclear factor E2-related factor 2 (Nrf2) signaling pathways in vitro. Honokiol suppressed MAFLD via activating the Nrf2 signaling pathway to play an antioxidant and anti-inflammatory role. Also, HNK regulates Nrf2 and RIPK3 signaling pathways to mitigate MAFLD.
Conclusion:
Our results showed that HNK may suppress the oxidative stress and inflammation in MAFLD via activation of Nrf2 signaling pathway.
Insights
Honokiol (HNK) shows promise in treating metabolic-associated fatty liver disease (MAFLD). This study found HNK effectively reduces liver fat, oxidative stress, and inflammation by activating the Nrf2 signaling pathway.
Area of Science:
- Hepatology
- Molecular Biology
- Pharmacology
Background:
- Metabolic-associated fatty liver disease (MAFLD) is a prevalent global health concern.
- Current therapeutic options for MAFLD are limited, necessitating novel treatment strategies.
Purpose of the Study:
- To investigate the efficacy of Honokiol (HNK) in mitigating MAFLD in vitro.
- To elucidate the underlying molecular mechanisms of HNK's protective effects.
Main Methods:
- MAFLD model established using LO2 cells and palmitic acid (PA).
- Assessed HNK's effects using Oil Red O staining, CCK-8 assay, qRT-PCR, and Western blot.
- Analyzed oxidative stress markers (ROS, MDA, CAT, SOD) and inflammatory cytokines (IL-1β, IL-6, TNF-α).
Main Results:
- Honokiol (50 μmol/L) effectively inhibited lipidosis and oxidative stress in MAFLD models.
- HNK mitigated MAFLD by activating the nuclear factor E2-related factor 2 (Nrf2) signaling pathway.
- HNK demonstrated antioxidant and anti-inflammatory roles by regulating Nrf2 and RIPK3 signaling.
Conclusions:
- HNK shows potential as a therapeutic agent for MAFLD.
- Activation of the Nrf2 signaling pathway is a key mechanism by which HNK exerts its protective effects against MAFLD-associated oxidative stress and inflammation.
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