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

Area of Science:

• Environmental Health
• Pulmonology
• Pharmacology

Background:

• Particulate matter (PM) exposure is a significant environmental risk factor for various lung pathologies.
• PM-induced lung injury is characterized by inflammation, apoptosis, and altered autophagy.
• Effective therapeutic strategies for PM-induced lung injury remain a critical unmet need.

Purpose of the Study:

• To investigate the protective effects and underlying mechanisms of dihydroartemisinin (DHA) against PM-induced lung injury.
• To evaluate DHA's impact on inflammatory responses, apoptosis, and autophagy in the context of PM exposure.

Main Methods:

• Lung injury was induced using PM particles both *in vivo* and *in vitro*.
• Histopathological analysis (H&E staining) assessed airway wall thickening and inflammatory cell infiltration.
• Inflammatory markers, apoptosis-related proteins (Bax, Bcl-2, cleaved-Caspase-3), autophagy markers (LC3-II, Beclin-1), and NF-κB signaling pathway activation (p-p65) were quantified.

Main Results:

• DHA treatment significantly alleviated PM-induced lung injury, as evidenced by reduced airway inflammation and cell infiltration.
• DHA demonstrated potent anti-inflammatory effects, decreasing key cytokines (IL-6, IL-8, IL-1β) by approximately 50%.
• DHA inhibited apoptosis by downregulating Bax and cleaved-Caspase-3, while promoting autophagy by reducing LC3-II and Beclin-1 levels, and suppressed NF-κB pathway activation.

Conclusions:

• Dihydroartemisinin (DHA) confers protection against particulate matter (PM)-induced lung injury.
• DHA exerts its protective effects through a combination of anti-inflammatory, anti-apoptotic, and autophagy-modulating mechanisms.
• DHA represents a promising therapeutic candidate for managing PM-induced lung injury.