Sulforaphane Attenuates PM2.5-Induced Chronic Obstructive Pulmonary Disease by Modulation of Nrf2 Activating and EGFR/PI3K/AKT Signaling - PubMed
5 hours ago
- #COPD
- #Nrf2 signaling
- #Sulforaphane
- Sulforaphane (SFN) shows prophylactic and therapeutic effects on PM2.5-induced chronic obstructive pulmonary disease (COPD).
- SFN attenuates lung injury, inflammation, mucus hypersecretion, and redox stress caused by PM2.5 exposure.
- Mechanistically, SFN activates the Nrf2 signaling pathway, reducing reactive oxygen species (ROS) generation.
- Network pharmacology and molecular docking identify EGFR as a key target of SFN.
- SFN binds to EGFR and suppresses the EGFR/PI3K/AKT signaling pathway, contributing to its protective effects.
- In a rat model, SFN provides therapeutic benefits primarily through EGFR/PI3K/AKT inhibition.
- The study highlights SFN's dual mechanism via Nrf2 activation and EGFR/PI3K/AKT inhibition for COPD treatment.