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Endothelial cell injury in vascular arterial walls plays a crucial role in the pathological process of atherosclerosis. Pterostilbene, a stilbenoid chemically related to resveratrol, has anti-inflammatory, anti-apoptosis and antioxidant properties. However, the underlying mechanisms mediated by pterostilbene in regards to endothelial cell injury in vascular arterial walls are not fully understood. The purpose of the present study was to investigate the benefits of pterostilbene in a rat model of atherosclerosis. The possible mechanism of pterostilbene was also analyzed in regards to endothelial cell injury in vascular arterial walls in vitro. A rat model of atherosclerosis was established using endothelial injury of the iliac arteries. CCK-8 assay, TUNEL, immunofluorescence, western blot analysis and hematoxylin and eosin (H&E) staining were used to analyze the role of pterostilbene in the pathological processes of atherosclerosis. In vivo results showed that pterostilbene decreased cholesterol (CHO), high-density lipoprotein cholesterol (HDL-C), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) in plasma and attenuated interleukin (IL)-1, tumor necrosis factor (TNF)-α and IL-6 and oxidative stress injury in serum in the experimental animals. Pterostilbene treatment reduced atherogenesis, aortic plaques, macrophage infiltration and apoptosis of vascular arterial walls in the atherosclerosis rat model. In vitro assay demonstrated that pterostilbene administration increased viability of the endothelial cells, attenuated oxidative stress injury and apoptosis of endothelial cells. The results found that pterostilbene regulated endothelial cell apoptosis via the Nrf2-mediated TLR-4/MyD88/NF-κB pathway. In conclusion, data from the present study revealed that pterostilbene protects rats against atherosclerosis by regulation of the Nrf2-mediated TLR-4/MyD88/NF-κB pathway. [ABSTRACT FROM AUTHOR]

Daidzein has been found to significantly inhibit the proliferation of lung cancer cells, while its potential molecular mechanisms remain unclear. To determine the molecular mechanism of daidzein on lung cancer cells, the Capital Bio Technology Human long non-coding (lnc) RNA Array v4, 4×180K chip was used to detect the gene expression profiles of 40,000 lncRNAs and 34,000 mRNAs in a human cancer cell line. Reverse transcription-quantitative (RT-q) PCR analysis was performed to detect the expression levels of target lncRNA and mRNAs in the H1299 cells treated with and without daidzein, using the lncRNA and mRNA gene chip. Bioinformatics analysis was performed to determine the differentially expressed genes from the results of the chip assays. There were 119 and 40 differentially expressed lncRNAs and mRNAs, respectively, that had a 2-fold change in expression level. A total of eight lncRNAs were upregulated in the H1299 lung cancer cells, while 111 lncRNAs were downregulated. Furthermore, five mRNAs were upregulated, and 35 mRNAs were downregulated. A total of six differentially expressed lncRNAs (ENST00000608897.1, ENST00000444196.1, ENST00000608741.1, XR_242163.1, ENST00000505196.1 and ENST00000498032.1) were randomly selected to validate the microarray data, which were consistent with the RT-qPCR analysis results. Differentially expressed mRNAs were enriched in important Gene Ontology terms and Kyoto Encyclopedia of Genes and Genomes pathways. Taken together, the results of the present study demonstrated that daidzein affected the expression level of lncRNAs in lung cancer cells, suggesting that daidzein may have potential effects on lung cancer cells. [ABSTRACT FROM AUTHOR]