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2-Fluorofucose Attenuates Hydrogen Peroxide-Induced Oxidative Stress in HepG2 Cells via Nrf2/keap1 and NF-κB
Mengjue Tu1, Xingshuo Fan1, Jianan Shi1
1Department of Pharmacology, School of Pharmacy, Nantong University, Nantong 226001, China.
Abstract:
Fucosylation is one of the most important glycan terminal modifications that affects multiple biological activities of proteins. 2-Fluorofucose (2FF), its specific inhibitor, has recently been reported to reveal numerous biological effects by blocking fucosylation both in vitro and in vivo. The current study aimed to evaluate the effect of 2FF on hydrogen peroxide (H2O2)-induced oxidative damage in vitro. In our study, treatment with H2O2 increased the level of fucosylation, and 2FF improved the cell viability in H2O2-treated HepG2 cells. Our study also showed that 2FF significantly decreased the overproduction of reactive oxygen species (ROS) induced by H2O2 and the activities of catalase, glutathione and Mn-superoxide dismutase were remarkably increased by 2FF pretreatment. Furthermore, 2FF attenuated H2O2-induced early mitochondria dysfunction. The second part of the study revealed that 2FF enhanced antioxidant capacity by affecting Nrf2/keap1 and NF-κB signaling pathways in HepG2 cells. Being pretreated with 2FF significantly increased the nuclear translocation of Nrf2 and simultaneously promoted the expression of downstream proteins, such as HO-1 and NQO1. Moreover, 2FF remarkably suppressed the expression of inflammation-associated proteins. Taken together, these data suggest that 2FF might have a potential therapeutic effect for oxidative stress.
Insights
2-Fluorofucose (2FF) protects HepG2 cells from hydrogen peroxide (H2O2)-induced oxidative damage. This fucosylation inhibitor reduces reactive oxygen species (ROS) and enhances antioxidant defenses, suggesting therapeutic potential for oxidative stress.
Area of Science:
- Biochemistry
- Cell Biology
- Oxidative Stress Research
Background:
- Fucosylation is a critical glycan modification impacting protein function.
- 2-Fluorofucose (2FF) is a specific inhibitor of fucosylation with demonstrated biological effects.
- Hydrogen peroxide (H2O2) is a key inducer of cellular oxidative damage.
Purpose of the Study:
- To investigate the protective effects of 2FF against H2O2-induced oxidative damage in HepG2 cells.
- To elucidate the mechanisms underlying 2FF's antioxidant and anti-inflammatory actions.
- To evaluate 2FF's impact on key cellular signaling pathways involved in oxidative stress response.
Main Methods:
- HepG2 cells were treated with H2O2 and/or 2FF.
- Assessed cell viability, reactive oxygen species (ROS) levels, and antioxidant enzyme activities (catalase, glutathione, Mn-SOD).
- Analyzed mitochondrial function, Nrf2/Keap1, and NF-κB signaling pathways, including protein expression (HO-1, NQO1).
Main Results:
- 2FF treatment improved cell viability in H2O2-exposed HepG2 cells.
- 2FF significantly reduced H2O2-induced ROS overproduction and enhanced antioxidant enzyme activities.
- 2FF attenuated mitochondrial dysfunction and modulated Nrf2/Keap1 and NF-κB pathways, decreasing inflammation.
Conclusions:
- 2FF demonstrates significant protective effects against H2O2-induced oxidative stress in HepG2 cells.
- 2FF enhances cellular antioxidant capacity and mitigates inflammation via Nrf2 and NF-κB signaling.
- 2FF holds potential as a therapeutic agent for conditions associated with oxidative stress.
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