Ginkgolide C Alleviates Acute Lung Injury Caused by Paraquat Poisoning via Regulating the Nrf2 and NF‐κB Signaling Pathways

Le résumé fourni par la source

Paraquat (PQ), a highly toxic herbicide and primary attack for lung, results in severe acute lung injury (ALI) appeared as evident oxidative stress, inflammation, and apoptosis. Increasing evidence elucidates that nuclear factor erythroid‐2‐related factor 2 (Nrf2) and its associated nuclear factor‐κB (NF‐κB) exhibit many merits for protection of ALI by coordinating a fine‐turned response to oxidative stress, inflammation, and apoptosis. Ginkgolide C (GC) has been reported to be a safe and potent therapeutic agent against ALI. However, whether GC could protect ALI induced by PQ poisoning and the possible underlining mechanisms have remained not to be fully elucidated. A rat model of ALI and a model of acute type II alveolar epithelial cell (RLE‐6TN) injury constructed by exposure to PQ were applied to discuss the protective effect of GC. Furthermore, Nrf2 gene silencing RLE‐6TN cells were used to discuss the exact mechanism. We confirmed that GC significantly ameliorated the histopathological damages, ultrastructural changes, lung injury score, W/D ratio, and Hyp activity of lung tissue and inhibited polymorphonuclear neutrophil (PMN) infiltration after PQ poisoning. Further results revealed that GC remarkably activated Nrf2‐based cytoprotective system and inhibited NF‐κB‐induced inflammatory injury as well as apoptosis. Taken together, we concluded that GC preserved protection of PQ‐induced ALI via the Nrf2‐NF‐κB dependent signal pathway, which may provide us novel insights into the treatment strategies for PQ poisoning.

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