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Updated: Feb 12, 2026

Ischemia-reperfusion Model of Acute Kidney Injury and Post Injury Fibrosis in Mice
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Dl-3-n-Butylphthalide Inhibits Ferroptosis and Attenuates Sepsis-Associated Acute Kidney Injury by Activating the

Ke Wang, Yan Yan, Junjie Ma

    Clinical Laboratory
    |February 11, 2026
    PubMed
    Abstract

    Insights

    Dl-3-n-butylphthalide (NBP) protects against sepsis-associated acute kidney injury (SA-AKI) by activating the Nrf2/HO-1 pathway. This intervention improved kidney function and reduced oxidative stress in a mouse model.

    Area of Science:

    • Nephrology
    • Pharmacology
    • Biochemistry

    Background:

    • Sepsis-associated acute kidney injury (SA-AKI) is a critical condition with significant morbidity and mortality.
    • Understanding the molecular mechanisms underlying SA-AKI is crucial for developing effective therapeutic strategies.

    Purpose of the Study:

    • To investigate the protective effects of Dl-3-n-butylphthalide (NBP) on SA-AKI.
    • To elucidate the underlying mechanisms, particularly the role of the Nrf2/HO-1 pathway.

    Main Methods:

    • A mouse model of SA-AKI was established using lipopolysaccharide (LPS).
    • Mice were treated with NBP or ferrostatin-1 (Fer-1).
    • Renal function, oxidative stress markers, and protein expression of key pathway molecules (Nrf2, HO-1, GPX4, SLC7A11) were assessed.

    Main Results:

    • LPS administration significantly impaired renal function and increased oxidative stress.
    • LPS treatment led to downregulation of Nrf2, HO-1, GPX4, and SLC7A11.
    • NBP and Fer-1 treatments significantly reversed these detrimental effects, improving renal function and restoring marker levels.

    Conclusions:

    • Dl-3-n-butylphthalide (NBP) demonstrates significant protective effects against SA-AKI.
    • NBP exerts its protective effects by activating the Nrf2/HO-1 signaling pathway.
    • NBP represents a potential therapeutic agent for managing SA-AKI.

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