空氣汙染和人類的健康息息相關，其中影響最大的懸浮微粒(Particulate matter ,PM)。本研究目的是了解暴露於PM2.5 的細胞活力和功能是否受到影響，並研究在PM2.5環境下機械循環拉伸中基因表達和相關途徑的差異。我們發現暴露於PM2.5的細胞與對照組之間的細胞活力沒有顯著差異，但A549細胞的遷移和侵襲能力會增強。此外，我們通過次世代定序得到在PM2.5環境中機械循環拉伸細胞的差異表達譜並通過IPA得到相關訊號通路，這些通路大多與免疫、發炎相關。另外在心肌細胞方面，從實驗結果表示PM2.5誘導的氧化壓力可能會對細胞造成氧化損傷。我們指出PM2.5誘導的活性氧產生可能會活化與細胞炎症反應相關的NF-κB訊號。總體而言，這些結果有助於提高對與PM2.5 相關的毒理學機制的理解。;Particulate matter (PM) has been associated with adverse health effects in exposed population. The aim of this study was to understand whether the viability and function of cells exposed to PM2.5 were affected and to study differences in gene expression and related pathways in mechanical cyclic stretching. We found no significant difference in cell viability between cells exposed to PM2.5 and the control group, but the invasion and migration ability of A549 cells exposed to PM2.5 were significantly increased. In addition, we obtained differential gene expression profiles of cells exposed to PM2.5 during mechanical cyclic stretching by NGS (next generation sequencing) and obtained relevant pathway analysis by IPA (ingenuity pathway analysis). The results showed that PM2.5 induced gene alteration were enriched in inflammation and immune pathway. In terms of the human cardiomyocyte cells, the results showed that PM2.5-induced oxidative stress may cause cell oxidative damage. We indicated that PM2.5 induced reactive oxygen species (ROS) generation might activate NF-κB signaling associated with cell inflammation response. Overall, these results aid in improving understanding of the toxicological mechanisms related to PM2.5.
