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Background <p>Acute lung injury (ALI) is a severe inflammatory disorder characterized by disruption of the alveolar-capillary barrier, uncontrolled inflammatory response, and excessive oxidative stress. Atractylenolide II (ATR II), a key sesquiterpenoid compound isolated from the <i>Atractylodes macrocephala</i>, has been shown to exert significant anti-inflammatory and antioxidant effects in various disease models. However, its therapeutic potential in ALI and the underlying molecular mechanisms remain largely unexplored. The present study was designed to elucidate the underlying mechanisms by which ATR II mediates its effects in ALI.</p> Methods <p>Lipopolysaccharide (LPS)-stimulated human alveolar epithelial A549 cells were employed to establish an in vitro ALI model. EdU proliferation assay and flow cytometry were applied to evaluate cell proliferation and apoptotic rates, respectively. Inflammatory cytokines and oxidative stress levels were assessed by enzyme-linked immunosorbent assay (ELISA) and specific commercial assay kits. Additionally, the protein expression of apoptosis-related molecules and TNIP2/NF-κB pathway-associated proteins were assessed by western blotting. The mRNA level of TNIP2 was measured by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) .</p> Results <p>ATR II significantly promoted cell proliferation and reduced apoptosis in LPS-induced A549 cells a dose-dependent manner. Furthermore, ATR II effectively inhibited the release of inflammatory factors and alleviated oxidative stress in LPS-stimulated A549 cells. Mechanistic investigations demonstrated that ATR II modulated the TNIP2/NF-κB signaling pathway: specifically, it upregulated TNIP2 protein expression, decreased phosphorylated p65 (p-p65) levels, and reduced the p-p65/p65 ratio. Knockdown of TNIP2 partially abrogated the protective effects of ATR II in LPS-exposed A549 cells.</p> Conclusion <p>Our findings revealed that ATR-II exerts protective effects against LPS-induced ALI in alveolar epithelial cells by regulating the TNIP2/NF-κB pathway. These results identified ATR-II as a potential therapeutic agent for the treatment of ALI.</p>

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Atractylenolide II alleviates LPS-induced acute lung injury in A549 cells via the TNIP2/NF-κB pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月16日

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  • Lixia Yu,
  • Huan Chen,
  • Xue Chen,
  • Yougang Ke,
  • Feng Fang,
  • Peng Ren,
  • Yisheng Wang

摘要

Background

Acute lung injury (ALI) is a severe inflammatory disorder characterized by disruption of the alveolar-capillary barrier, uncontrolled inflammatory response, and excessive oxidative stress. Atractylenolide II (ATR II), a key sesquiterpenoid compound isolated from the Atractylodes macrocephala, has been shown to exert significant anti-inflammatory and antioxidant effects in various disease models. However, its therapeutic potential in ALI and the underlying molecular mechanisms remain largely unexplored. The present study was designed to elucidate the underlying mechanisms by which ATR II mediates its effects in ALI.

Methods

Lipopolysaccharide (LPS)-stimulated human alveolar epithelial A549 cells were employed to establish an in vitro ALI model. EdU proliferation assay and flow cytometry were applied to evaluate cell proliferation and apoptotic rates, respectively. Inflammatory cytokines and oxidative stress levels were assessed by enzyme-linked immunosorbent assay (ELISA) and specific commercial assay kits. Additionally, the protein expression of apoptosis-related molecules and TNIP2/NF-κB pathway-associated proteins were assessed by western blotting. The mRNA level of TNIP2 was measured by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) .

Results

ATR II significantly promoted cell proliferation and reduced apoptosis in LPS-induced A549 cells a dose-dependent manner. Furthermore, ATR II effectively inhibited the release of inflammatory factors and alleviated oxidative stress in LPS-stimulated A549 cells. Mechanistic investigations demonstrated that ATR II modulated the TNIP2/NF-κB signaling pathway: specifically, it upregulated TNIP2 protein expression, decreased phosphorylated p65 (p-p65) levels, and reduced the p-p65/p65 ratio. Knockdown of TNIP2 partially abrogated the protective effects of ATR II in LPS-exposed A549 cells.

Conclusion

Our findings revealed that ATR-II exerts protective effects against LPS-induced ALI in alveolar epithelial cells by regulating the TNIP2/NF-κB pathway. These results identified ATR-II as a potential therapeutic agent for the treatment of ALI.