Dihydroartemisinin attenuates PM-induced lung injury by inhibiting inflammation and regulating autophagy.

in Frontiers in public health by Lingjing Liu, Jingli Li, Yincong Xue, Shuying Xie, Nian Dong, Chengshui Chen

TLDR

  • The study shows that dihydroartemisinin (DHA) alleviates lung injury induced by particulate matter (PM) in mice by reducing inflammation, apoptosis, and regulating autophagy.
  • DHA may be a potential therapeutic option for improving PM-induced lung injury, and further studies could investigate its optimal use.

Abstract

The study investigates the effects and mechanisms of dihydroartemisinin (DHA) in mitigating lung injury induced by particulate matter (PM). The lung injury model was induced by PM particlesand. Hematoxylin and Eosin (H&E) staining was utilized for the detection of the thickening of airway wall and the infiltration of inflammatory cells in mouse lung tissue. The expressions of inflammatory factors were detected in alveolar lavage fluid and cell supernatant. TUNEL (Terminal deoxynucleotidyl transferase dUTP nick end labeling) staining, Caspase-1, Bcl-2-associated X protein (Bax), B-cell lymphoma 2 (Bcl-2), microtubule-associated protein 1 light chain 3-II (LC3-II) and Belcin-1 were used to observe the apoptosis and autophagy related expressions in mouse lung tissue, and p-p65 was detected by immunofluorescence. H&E staining revealed DHA alleviates PM-induced lung injury. Moreover, DHA reduced IL-6, IL-8, and IL-1β levels by ~50% (< 0.05), highlighting its anti-inflammatory effects. Furthermore, immunohistochemistry showed that DHA treatment inhibited the pro-apoptotic expression of Bax/BCL2 and cleaved-Caspase-3, respectively. In addition, immunofluorescence staining revealed that the LC3-II and Beclin-1 levels dramatically increased in the PM group compared to Control group, but greatly reduced by DHA. Further, we found that DHA inhibited the activation of the NF-KB signaling pathway. DHA protects against PM-induced lung injury through anti-inflammatory, anti-apoptotic, and autophagy-regulating mechanisms, offering a potential drug option for improving PM-induced lung injury.

Overview

  • The study investigates the effects of dihydroartemisinin (DHA) in mitigating lung injury induced by particulate matter (PM) in mice.
  • The lung injury model was induced by PM particles and lung tissue sections were stained with H&E to detect airway wall thickening and inflammatory cell infiltration.
  • The study aims to identify the mechanisms by which DHA protects against PM-induced lung injury and its potential as a therapeutic option for PM-induced lung injury.

Comparative Analysis & Findings

  • DHA treatment alleviated PM-induced lung injury as revealed by H&E staining and reduced inflammatory factors IL-6, IL-8, and IL-1β by ~50% (< 0.05).
  • DHA inhibited the pro-apoptotic expression of Bax/BCL2 and cleaved-Caspase-3, and increased LC3-II and Beclin-1 levels to regulate autophagy.
  • DHA also inhibited the activation of the NF-KB signaling pathway, highlighting its anti-inflammatory effects.

Implications and Future Directions

  • The study suggests that DHA may be a potential therapeutic option for improving PM-induced lung injury due to its anti-inflammatory, anti-apoptotic, and autophagy-regulating mechanisms.
  • Future studies could investigate the optimal dosing and duration of DHA treatment for optimal protection against PM-induced lung injury.
  • Exploring the molecular mechanisms of DHA's effects on lung injury may provide insights into identifying novel therapeutic targets for PM-induced lung injury.
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