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<p>Acute lung injury (ALI) is a severe respiratory syndrome for which there is still a lack of effective treatment. Salvianolic acid A (Sal A) is a bioactive polyphenol extracted from <i>Salvia miltiorrhiza</i> Bunge, which has anti-inflammatory and antioxidant effects, but its role in ALI is unclear. We injected 50 µL LPS into the trachea of mice, and treated MLE-12 cells with 1&#xa0;µg/mL LPS to construct ALI mouse and cell model. The levels of genes and proteins was identified using RT‒qPCR, western blot and immunofluorescence. The damage of MLE-12 cells and mouse lung tissue was evaluated by CCK-8, ELISA, TUNEL and HE staining. Sal A treatment can significantly inhibit LPS-induced inflammation and apoptosis, and then inhibit MLE-12 cell damage and ALI progression. From a mechanistic standpoint, Sal A promotes the expression of LC3 II/I and Beclin1, suppresses p62 expression, increases cell autophagy, and suppresses LPS-induced inflammatory cytokines IL-6, IL-1β, and TNF-α expression, ultimately reducing LPS-induced inflammation in lung epithelial cells and alleviating ALI progression. The main function of Sal A is to achieve this by inhibiting the expression of miR-217-5p and thereby promoting the expression of FOXO1. Our research results may provide a new target for the treatment of ALI with Sal A.</p>

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Salvianolic Acid A Relieves Acute Lung Injury by Promoting the Expression of FOXO1 and Activating Autophagy Through the Inhibition of miR-217-5p

  • 期刊论文

  • 发表日期：

    2025年11月15日

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  • Xia Liu,
  • Yanping Shi,
  • Li Huang,
  • Hongbo Chen,
  • Raofei Fan,
  • Hongzhong Zhang,
  • Qiaofen Li,
  • Na Yan,
  • Maiding He,
  • Yonghua Yang

摘要

Acute lung injury (ALI) is a severe respiratory syndrome for which there is still a lack of effective treatment. Salvianolic acid A (Sal A) is a bioactive polyphenol extracted from Salvia miltiorrhiza Bunge, which has anti-inflammatory and antioxidant effects, but its role in ALI is unclear. We injected 50 µL LPS into the trachea of mice, and treated MLE-12 cells with 1 µg/mL LPS to construct ALI mouse and cell model. The levels of genes and proteins was identified using RT‒qPCR, western blot and immunofluorescence. The damage of MLE-12 cells and mouse lung tissue was evaluated by CCK-8, ELISA, TUNEL and HE staining. Sal A treatment can significantly inhibit LPS-induced inflammation and apoptosis, and then inhibit MLE-12 cell damage and ALI progression. From a mechanistic standpoint, Sal A promotes the expression of LC3 II/I and Beclin1, suppresses p62 expression, increases cell autophagy, and suppresses LPS-induced inflammatory cytokines IL-6, IL-1β, and TNF-α expression, ultimately reducing LPS-induced inflammation in lung epithelial cells and alleviating ALI progression. The main function of Sal A is to achieve this by inhibiting the expression of miR-217-5p and thereby promoting the expression of FOXO1. Our research results may provide a new target for the treatment of ALI with Sal A.