Ginkgo Biloba extract improved Paraquat-induced pulmonary fibrosis via inhibiting p38 MAPK pathway

Objective This study aims to reveal the potential mechanism of Ginkgo Biloba extract (GBE) in alleviating pulmonary fibrosis. Methods We examined cell viability, PINK1, Parkin and LC3 II/I ratio in PQ-stimulated rat alveolar epithelial type II cells (RLE-6TN) receiving GBE treatment. LC3 enrichment in mitochondria was detecting the immunofluorescence co-staining of LC3 and TOMM20. Then, epithelial mesenchymal transition (EMT) was evaluated by -SMA and E-cadherin using immunofluorescence. Also, p-p38 and p38 were measured to evaluate p38 MAPK pathway using western blot. SB203580 was used to inhibiting p38 in RLE-6TN cells. The changes in histopathological alteration, -SMA, E-cadherin, PINK1, Parkin, LC3 II/I ration and collagen deposition was also investigated in rats with PQ stimulation and GBE treatment. Results PQ caused the decrease in cell viability and E-cadherin, and the increase in LC3 enrichment, -SMA, PINK1, Parkin and LC3 II/I ratio (P<0.05). p-p38 was increased after PQ stimulation (P<0.05). In PQ-stimulated RLE-6TN cells, GBE elevated cell viability and E-cadherin and reduced LC3 enrichment, -SMA, PINK1, Parkin, LC3 II/I ratio and p-p38 (P<0.05). Both of GBE and SB203580 significantly reversed PQ-induced changes abovementioned in cells. Rats with PQ stimulation developed the increase in hydroxyproline activity, -SMA, p-p38, PINK1, Parkin LC3 II/I ratio and the decrease in E-cadherin (P<0.05). GBE significantly reversed PQ-induced changes abovementioned in rats. GBE mitigated inflammatory infiltrates, alveolar wall thickening and collagen deposition in rats undergoing PQ stimulation. Conclusion GBE significantly inhibited EMT and mitophagy in alveolar epithelial type II cells exposed to PQ via suppressing p38 MAPK pathway.