Sodium Benzoate Induces Fat Accumulation and Reduces Lifespan via the SKN-1/Nrf2 Signaling Pathway: Evidence from the Caenorhabditis elegans Model

苯甲酸钠通过 SKN-1/Nrf2 信号通路诱导脂肪堆积并缩短寿命:来自秀丽隐杆线虫模型的证据

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作者:Jiah D Lee, Jiwoo Lee, Jerry Vang, Xiaoping Pan

Background

Sodium benzoate (SB) is widely used in food products, cosmetics, and medical solutions due to its antimicrobial properties. While it is generally considered safe and has potential neuroprotective benefits, SB has also been linked to adverse effects, including hepatic oxidative stress and inflammation. However, the potential effects of SB on obesity and lifespan remain poorly understood. Objectives: In this study, we investigated the effects of SB on fat accumulation and lifespan using the nematode Caenorhabditis elegans (C. elegans) as a model system.

Conclusion

These findings suggest that SB may induce fat accumulation and reduce lifespan by inhibiting the oxidative stress-mediated SKN-1 signaling pathway.

Methods

Wild-type worms were exposed to various SB concentrations (0%, 0.0004%, 0.0008%, 0.004%, and 0.1%) and 0.016% glucose as a positive control for 72 h in liquid or on NGM agar plates. Result: Fat accumulation was assessed through the Oil Red O staining, which revealed that SB induced more fat accumulation compared to vehicle control, even at low concentrations, including the dosage of 0.0004%. Lifespan analysis also demonstrated that SB significantly reduced lifespan in wild-type worms, even at low concentrations. Further investigations found that SKN-1 (an Nrf2 homolog) is necessary for SB-induced fat accumulation and lifespan reduction. Moreover, SB inhibited the nuclear localization of SKN-1 under oxidative stress conditions.

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