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jdk.nashorn.api.scripting.NashornScriptEngine.getInterface(java.lang.Object,java.lang.Class) public java.lang.Object jdk.nashorn.api.scripting.NashornScriptEngine.getInterface(java.lang.Class) public java.lang.Object jdk.nashorn.api.scripting.NashornScriptEngine.invokeMethod(java.lang.Object,java.lang.String,java.lang.Object[]) throws javax.script.ScriptException,java.lang.NoSuchMethodException public java.lang.Object jdk.nashorn.api.scripting.NashornScriptEngine.invokeFunction(java.lang.String,java.lang.Object[]) throws javax.script.ScriptException,java.lang.NoSuchMethodException public javax.script.Bindings jdk.nashorn.api.scripting.NashornScriptEngine.createBindings() public java.lang.Object javax.script.AbstractScriptEngine.get(java.lang.String) public void javax.script.AbstractScriptEngine.put(java.lang.String,java.lang.Object) public javax.script.ScriptContext javax.script.AbstractScriptEngine.getContext() public java.lang.Object 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Journal of Southern Medical University ›› 2026, Vol. 46 ›› Issue (5): 1006-1017.doi: 10.12122/j.issn.1673-4254.2026.05.04

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Ultrafine Xiebai powder alleviates lipopolysaccharide-induced acute lung injury in mice by suppressing ferroptosis and modulating the NF-κB/STAT3 signaling axis

Jinchao ZHU1(), Ningning SHAO2, Zeyu HUANG2, Yanqing LIU1, Xiangyan MENG1, Ziquan LIU1, Yujie SUN3, Jinrui DONG2(), Haojun FAN1()   

  1. 1.Key Laboratory of Key Technology and Equipment of the Ministry of Emergency Management of Medical Rescue, School of Disaster and Emergency Medicine, Tianjin University, Tianjin 300072, China
    2.School of Medicine, Tianjin University, Tianjin 300072, China
    3.Hainan Vandailan Biopharmaceutical Technology Co. , Ltd. , Chengmai 571900, China
  • Received:2025-10-27 Online:2026-05-20 Published:2026-05-27
  • Contact: Jinrui DONG, Haojun FAN E-mail:zjc_128@tju.edu.cn;jinrui_dong@tju.edu.cn;haojunfan86@163.com
  • Supported by:
    National Natural Science Foundation of China(82200655)

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Abstract:

Objective To investigate the protective effects of ultrafine Xiebai powder (UXP) against lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice and the underlying mechanism. Methods Fifty-four male C57BL/6 mice were randomized into 9 groups, including a control group and 8 intratracheal LPS instillation-induced ALI model groups gavaged with saline, dexamethasone (DEX, 1 mg/kg), or 100, 250, or 500 mg/kg UXP or granule Xiebai powder (n=6) for 6 consecutive days, starting on the day of modeling. After the treatment, the lung wet-to-dry (W/D) ratios were determined, inflammatory cytokines in bronchoalveolar lavage fluid (BALF) were measured by ELISA, and inflammatory cell infiltration was assessed by flow cytometry. Histopathological injury of the lungs was observed using HE staining, and pulmonary SOD, MDA, and GSH levels were determined. Pulmonary mRNA expressions of inflammatory mediators were quantified by RT-qPCR, and NF‑κB and STAT3 activation was analyzed using Western blotting; mitochondrial ultrastructure was examined with transmission electron microscopy. In a LPS-stimulated BEAS-2B cell model, the effects of UXP and DEX were assessed on cell viability, apoptosis, reactive oxygen species (ROS), mitochondrial function, lipid peroxidation, and ferrous iron levels. Results The LPS-challenged mice exhibited a higher lung W/D ratio and increased BALF cytokine levels and inflammatory cell counts with pronounced lung inflammation and tissue damage, lowered SOD and GSH levels, elevated MDA levels, increased mRNA expressions of inflammatory mediators and the p-NF‑κB/NF‑κB and p-STAT3/STAT3 ratios, and obvious mitochondrial damages. UXP markedly alleviated these changes with an efficacy comparable to DEX. In LPS-stimulated BEAS-2B cells, UXP significantly improved cell viability, redcued cell apoptosis and ROS accumulation, preserved mitochondrial integrity, and reduced lipid peroxidation and ferroptosis-associated changes. Conclusion UXP has strong protective effects against LPS-induced ALI in mice possibly by suppressing inflammation, oxidative stress, ferroptosis, and apoptosis, modulating the NF‑κB/STAT3 signaling axis, and maintaining mitochondrial integrity.

Key words: ultrafine Xiebai powder, acute lung injury, inflammation, oxidative stress, ferroptosis