STUDIES ON CYANIDIN-3-O-GLUCOSIDE REGULATING AUTOPHAGY AND APOPTOSIS OF PM2.5-INDUCED ACUTE LUNG INJURY CELLS VIA AMPK SIGNALING PATHWAY

Objective: This study explored the relationship between PM2.5-induced acute lung injury and AMPK/mTOR signaling pathway, autophagy, apoptosis and lung inflammation, as well as the protective mechanism of Cyanidin-3-o-glucoside pre-administration. Methods: Through studying lung tissue TUNEL fluorescence, apoptosis index, apoptosis pathway proteins (Bax, Bcl 2, caspase 3, cleaved caspase 3, PARP 1, and cleaved PARP 1) and inflammation pathway proteins (p-IκBα, p-p65), the paper explored the effect of Cyanidin-3-o-glucoside on PM2.5-induced apoptosis and inflammation pathways of acute lung injury. Secondly, by observing the pulmonary edema index (dry-wet ratio), HE staining of lung tissue, AAV2/6-LC3-GFP-RFP vector in vivo monitoring of autophagy flow, autophagy proteins (LC3B, Beclin 1) and AMPK/mTOR pathway protein (AMPK, P-AMPK, mTOR, p-mTOR, and p-ULK 1), the paper studied the effects of Cyanidin-3-o-glucoside on PM2.5-induced autophagy and AMPK/mTOR pathway in acute lung injury cells. Results: Cyanidin-3-o-glucoside can inhibit the Bcl2-Bax/caspase 3/caspase PARP 1 apoptosis pathway, reduce the TUNEL fluorescence apoptotic index, and then inhibit the downstream NF-κB pathway, reduce lung inflammation, and protect from PM2.5-induced acute lung injury. Conclusion: Prophylactic administration of Cyanidin-3-o-glucoside activates autophagic flux through AMPK/mTOR/ULK 1 pathway, inhibits cell apoptosis, reduces lung inflammation, and protects from PM2.5-induced acute lung injury.