ArticleActa biochimica et biophysica Sinica2024
Germacrone ameliorates acute lung injury induced by intestinal ischemia-reperfusion by regulating macrophage M1 polarization and mitochondrial defects.
Article in Acta biochimica et biophysica Sinica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Nrf2/UBE3B protects against acute lung injury by inhibiting ferritinophagy through the ubiquitination of NCOA4.Biology direct · 2025Article
- Identification and validation of mitochondrial-related genes in intestinal ischemia-reperfusion injury based on WGCNA and machine learning.Frontiers in molecular biosciences · 2025Article
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Abstract
Intestinal ischemia-reperfusion (I/R) injury severely affects the lungs. Germacrone (Ger) possesses anti-inflammatory and antioxidant properties. However, it is unclear whether it protects the lungs from I/R injury. In this study, we elucidate the mechanisms by which Ger protects lungs from I/R injury. C57BLKS/J male mice are subjected to I/R injury via complete clamping of the superior mesenteric artery. Ger is administered before intestinal I/R. Mitochondrial morphology is observed via electron microscopy. The histopathology of the lung tissues is monitored via hematoxylin-eosin and immunofluorescence staining. The mitochondrial oxygen consumption rate is measured via an XF96 extracellular flux analyzer. In the I/R mouse model, lung specimens present significant lung damage accompanied by increases in the levels of collagen III, vimentin, and α-SMA in lung tissues. After treatment with Ger, lung impairment and fibrosis in I/R-induced acute lung injury (ALI) model mice are restored, suggesting that Ger improves I/R-ALI. In addition, Ger administration decreases the release of inflammatory factors such as IL-1β, IL-6, and COX2, as well as the expressions of M1 macrophage markers, facilitating cell survival in the I/R-ALI model. Additionally, Ger (EC50: 47.16 μM) ameliorates mitochondrial dysfunction by increasing I/R-ALI-induced apoptosis, increasing the expression of SIRT1, and reducing the levels of HIF1-α, Nrf2, and OGG1 in MLE-12 cells. Ger may affect macrophage polarization and improve subsequent mitochondrial defects through the SIRT1-HIF1α-Nrf2 signaling pathway in MLE-12 cells, which ultimately improves lung function and lung inflammation in the I/R-ALI model.
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