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IF was used to measure NF‑κB p65 nuclear translocation. The results revealed that GEN significantly decreased the expression of inflammation‑associated vascular factors in LPS‑treated C57BL/6 mice, including TNF‑α, IL‑6, iNOS, NF‑κB p65 and miR‑21. Furthermore, miR‑21 antagomir enhanced the anti‑inflammatory effects of GEN. In LPS‑induced VECs, miR‑21 mimic increased inflammation‑associated factor expression and attenuated the anti‑inflammatory effects of GEN, whereas miR‑21 inhibitor induced opposing effects. Therefore, the results of the present study suggested that GEN inhibited chronic vascular inflammatory response in mice, which may be associated with the inhibition of VEC inflammatory injury via the miR‑21/NF‑κB p65 pathway.Trienones are curcuminoid analogues and are minor constituents in the rhizomes of numerous Curcuma plant species. Studies investigating the biological activities of trienones, particularly their anti‑inflammatory activities, are limited. In the present study, the trienone 1,7‑bis(4‑hydroxy‑3‑methoxyphenyl)‑1,4,6‑heptatrien‑3‑one (HMPH) was structurally modified from curcumin using a novel and concise method. HMPH was shown to exhibit potential anti‑inflammatory effects on lipopolysaccharide (LPS)‑activated RAW264.7 macrophages. Furthermore, LPS‑induced nitric oxide secretion in RAW264.7 cells was markedly and dose‑dependently inhibited by HMPH; in addition, HMPH had a greater efficacy compared with curcumin. This inhibition was accompanied by the suppression of inducible nitric oxide synthase and cyclooxygenase‑2 expression, as well as pro‑inflammatory cytokine secretion. To elucidate the molecular mechanism underlying the anti‑inflammatory effects of HMPH, the effects of this compound on nuclear factor‑κB (NF‑κB) translocation were assessed. HMPH significantly inhibited the translocation of p65 NF‑κB into the nucleus to a greater extent than curcumin, thus indicating that HMPH has more potent anti‑inflammatory activity than curcumin. In addition, an in silico modelling study revealed that HMPH possessed stronger binding energy to myeloid differentiation factor 2 (MD2) compared with that of curcumin, and indicated that the anti‑inflammatory effects of HMPH may be through upstream inhibition of the inflammatory pathway. In conclusion, HMPH may be considered a promising compound for reducing inflammation via targeting p65 NF‑κB translocation and interfering with MD2 binding.Gastric cancer (GC) is one of the most common malignancies of the digestive system. In diffuse‑type GC, differentiation is relatively poor, and the probability of distant metastasis and lymph node metastasis is high, resulting in poor clinical prognosis. The purpose of this study was to identify specific genes that can predict the prognosis of different types of GC. Differentially expressed genes (DEGs) were screened in the GSE62254 dataset obtained from the Gene Expression Omnibus using the ‘limma’ and ‘survival’ R packages. A total of 355 survival‑related DEGs were selected according to specific screening criteria, of which 293 were associated with diffuse‑type GC and 62 with intestinal‑type GC. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes were used for functional annotation and pathway enrichment analysis of DEGs. Ceralasertib cell line Using protein‑protein interaction networks and Cytoscape software, three hub genes were identified in diffuse‑type GC‑associated DEGs, including angiotensinogen (AGT), C‑X‑C motif chemokine ligand 12 (CXCL12) and adrenoceptor β2 (ADRB2). Immunohistochemical staining and reverse transcription‑quantitative PCR revealed that the expression levels of the three genes in diffuse‑type GC samples were upregulated compared with in intestinal‑type GC samples. Kaplan Meier analysis indicated that a higher expression levels of these three hub genes were associated with a poorer prognosis of diffuse‑type GC. In summary, the present findings suggested that AGT, CXCL12 and ADRB2 might contribute to the progression of diffuse‑type GC, and could serve as potential biomarkers or therapeutic targets for this disease.Long non‑coding (lnc)RNAs serves an important role in the occurrence and development of hepatic fibrosis. lncRNA AK021443 is highly expressed in hepatocellular carcinoma (HCC) and promotes HCC cell proliferation, invasion and migration. The present study aimed to investigate the effect of AK021443 on hepatic fibrosis. AK021443 was overexpressed in the human LX‑2 hepatic stellate cell (HSC) line using a plasmid to observe its effect on hepatic fibrosis in vitro. A Cell Counting Kit‑8 assay was performed to assess cell proliferation, whereas cell cycle distribution and related proteins were analyzed via flow cytometry and western blotting, respectively. The protein expression levels of epithelial‑mesenchymal transition (EMT)‑associated and extracellular matrix (ECM) proteins were also analyzed via western blotting. Immunofluorescence was conducted to observe the generation of collagen1, and the activity of inflammatory factors and reactive oxygen species (ROS) was also analyzed. Compared with the pcDNA group, AK021443 overexpression significantly promoted cell proliferation, enhanced the transition of cells from G1 to S phase and increased the expression of cyclin‑dependent kinase 2 and cyclin D1, but reduced the p21 protein expression levels. In addition, EMT capabilities, ECM deposition and the generation of collagen1 were increased by AK021443 overexpression compared with the pcDNA group. Moreover, AK021443 overexpression significantly increased the release of inflammatory cytokines, including TGF‑β, interleukin‑1β, platelet derived growth factor, epidermal growth factor and ROS, compared with the pcDNA group. In conclusion, the present study suggested that AK021443 overexpression increased HSC proliferation, activation and the proinflammatory response, indicating the potential role of AK02144 in aggravating hepatic fibrosis.MicroRNAs (miRs) are essential regulators of atherosclerosis (AS) development; however, the pathogenic roles of miR-140-5p during AS development are not completely understood. The present study investigated the effects of miR‑140-5p on human vascular smooth muscle cells (VSMCs) and its target gene. miR-140-5p and roundabout guidance receptor 4 (ROBO4) mRNA expression levels were determined by performing reverse transcription-quantitative PCR. ROBO4 protein expression levels were analyzed via western blotting. Cell viability, migration, invasion and apoptosis were evaluated by conducting Cell Counting Kit-8, Transwell and flow cytometry assays, respectively. The binding of miR-140-5p to ROBO4 mRNA was verified using the dual-luciferase reporter assay. miR-140-5p was highly expressed in the plaque-containing artery tissues of patients with AS compared with healthy control tissues. Oxidized-low density lipoprotein (ox-LDL) treatment increased miR-140-5p expression and decreased ROBO4 expression in human VSMCs, which promoted VSMC viability, migration and invasion, but suppressed apoptosis compared with the control group.