PM induces the abnormal lipid metabolism and leads to atherosclerosis via Notch signaling pathway in rats.

PM can affect the lipid metabolism and cause atherosclerosis. Abnormal lipid metabolism is a sever risk factor of atherosclerosis and the underlying molecular mechanism still remains unclear. In this study, GPL16956 Agilent-045997 Arraystar human lncRNA microarray V3 (Probe Name Version) platform was used to detect the different genes of lipid metabolism between the normal arterial intima and advanced atherosclerotic plaque, which were downloaded from GEO database. A high-fat diet and vitamin D3 were administered to Wistar rats to establish the atherosclerotic model and another normal healthy 56 rats were used as the non-atherosclerotic exposure groups. The atherosclerotic rats and non-atherosclerotic rats were randomly divided into 4 PM groups (0, 1.5, 7.5, 37.5 mg/kg), respectively. The results of bioinformatics showed changes in the Notch1, Dll1, Hes1, LDLR and ABCG1 levels. PM exposure could produce damage to the physiological structure of the aorta, and aggravate atherosclerosis in rats from both non-atherosclerotic and atherosclerotic groups. With the increase of the exposure dose, the levels of TC and TG significantly increased. PM exposure significantly affected the expression levels of PPARγ, ABCA1, LDLR, CD36, SR-BI and SREBP2. PM exposure could also affect the expression levels of the Notch signaling pathways which was significantly correlated with the levels of TC and TG. The results proved that PM exposure could induce and aggravate the atherosclerosis in rats by disrupting lipid metabolism in which Notch signaling pathway may play a significant role.