ArticleInternational journal of medical sciences2026
Isoalantolactone Attenuates LPS-Induced Acute Lung Injury, an Effect Associated with Suppressed MAPK/STAT3 Activation and Epithelial-Mesenchymal Transition.
Article in International journal of medical sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Acute lung injury (ALI) is characterized by a high mortality rates and acute inflammation that compromises the epithelial and endothelial barriers of the respiratory system. Isoalantolactone (IsoA) is a natural compound derived from Methods: Human bronchial epithelial cells (HBEC3-KT and BEAS-2B) were stimulated with lipopolysaccharide (LPS) with or without IsoA to assess cytotoxicity and cytokine release. In vivo, female C57BL/6 mice were pretreated with IsoA (10-20 mg/kg, intraperitoneally) or vehicle 1 h before LPS challenge (1 mg/kg, intratracheally). At 4 h, lung tissues and bronchoalveolar lavage fluid (BALF) were collected for histopathology and to measure total protein, cellular composition, and cytokine levels (tumor necrosis factor-α [TNF-α], interleukin-6 [IL-6], monocyte chemoattractant protein-1 [MCP-1]); leukocyte subsets were quantified by multicolor flow cytometry. Lung homogenates were analyzed using Western blot for phosphorylated/total extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase 1/2 (JNK1/2), p38 MAPKs, STAT3, and EMT markers (E-cadherin, N-cadherin, snail). Results: In LPS-stimulated HBEC3-KT and BEAS-2B cells, IsoA significantly reduced IL-6 secretion. In the murine model of LPS-induced ALI, IsoA administration alleviated lung tissue damage, decreased inflammatory cell infiltration, and reduced IL-6 and TNF-α concentration in BALF and serum. Mechanistically, IsoA attenuated the phosphorylation of ERK, JNK, and p38 MAPKs and suppressed STAT3 activation in lung tissues. Furthermore, IsoA attenuated EMT, as evidenced by decreased N-cadherin and snail expressions and restored E-cadherin expression. Conclusions: IsoA alleviates LPS-induced ALI by reducing MAPK/STAT3 activation and EMT-associated epithelial injury. These findings suggest that IsoA may be a promising candidate for the targeted modulation of inflammatory lung injury, and that further preclinical and translational studies are justified.
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