Minxuan Peng

Flavonoids are a group of polyphenolic compounds, diverse in chemical structure and characteristics, found ubiquitously in plants. Until now, more than 9000 different flavonoid compounds were described in plants, where they play important biological roles by affecting several developmental processes. There has been increasing interest in the research of flavonoids from dietary sources, due to growing evidence of the versatile health benefits of flavonoids including anti-inflammatory, antioxidant, antiproliferative and anticancer activity, freeradical scavenging capacity, antihypertensive effects, coronary heart disease prevention and anti-human immunodeficiency virus functions. This paper reviews the current advances in flavonoids in food with emphasis on mechanism aspects on the basis of the published literature, which may provide some guidance for researchers in further investigations and for industries in developing practical health agents. Keywords: Flavonoids, mechanism, health benefits, review, polyphenolic compounds, antioxidant, antiproliferative, anticancer activity, freeradical scavenging capacity, antihypertensive effects

INTRODUCTION: This study aimed to reveal the potential mechanism of Ginkgo biloba extract (GBE) in alleviating pulmonary fibrosis. METHODS: We examined cell viability, PTEN-induced putative kinase 1 (PINK1), Parkin, and microtubule-associated protein 1 light chain 3 (LC3) II/I ratio in paraquat (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 α smooth muscle actin (α-SMA) and E-cadherin using immunofluorescence. Also, p-p38 and p38 were measured to evaluate p38 mitogen-activated protein kinase (MAPK) pathway using Western blot. SB203580 was used to inhibiting p38 in RLE-6TN cells. The changes in histopathological alteration, α-SMA, E-cadherin, PINK1, Parkin, LC3 II/I ratio, and collagen deposition were 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, α-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, α-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, α-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.