Sodium Propionate Attenuates the Lipopolysaccharide-Induced Epithelial–Mesenchymal Transition via the PI3K/Akt/mTOR Signaling Pathway

• DOI: 10.1021/acs.jafc.0c01302
• Publication Date: 2020-05-26T13:03:40Z
• Authors: Dan Chen; Yu-bao Qiu; Zhi-qi Gao; Ya-Xian Wu; Bin-bin Wan; Gang Liu; Jun-liang Chen; Qin Zhou; Ren-qiang Yu; Qing-feng Pang
• Keywords: Lipopolysaccharides; Lung Diseases; Male; 0303 health sciences; Epithelial-Mesenchymal Transition; TOR Serine-Threonine Kinases; Cadherins; Actins; 3. Good health; Mice; 03 medical and health sciences; Animals; Humans; Vimentin; Phosphatidylinositol 3-Kinase; Propionates; Proto-Oncogene Proteins c-akt; Signal Transduction

Short-chain fatty acids (SCFAs), especially propionate, originate from the fermentation of dietary fiber in gut and play a key role inhibiting pulmonary inflammation. Chronic inflammation may induce an epithelial–mesenchymal transition (EMT) alveolar epithelial cells result fibrotic disorders. This study was designed to investigate beneficial effect sodium propionate (SP) on lipopolysaccharide (LPS)-induced EMT. In cultured BEAS-2B cells, protein expression levels E-cadherin, α-smooth muscle actin (SMA), vimentin were 0.66 ± 0.20, 1.44 0.23, 1.32 0.21 LPS group vs 1.11 0.36 (P < 0.05), 1.04 0.30 0.96 0.13 0.01) + SP (mean standard deviation), respectively. Meanwhile, LPS-triggered inflammatory cytokines extracellular proteins also reduced by administration cells. Moreover, treatment attenuated inflammation, EMT, matrix (ECM) deposition, even fibrosis mouse EMT model. terms mechanism, LPS-treated exhibited higher level phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target rapamycin (mTOR) phosphorylation, which interrupted treatment. It is worth noting that blockade PI3K/Akt/mTOR signaling cascade LPS-evoked process These results suggest can block LPS-induced via inhibition cascade, provides basis for possible clinical use airway lung diseases.