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To explore the protective function and molecular mechanism of tribuloside in hydrogen peroxide-induced apoptosis and oxidative damage of human lens epithelial cells. Cells were divided into control group, hydrogen peroxide group, hydrogen peroxide+tribuloside 1 µg/ml group, hydrogen peroxide+tribuloside 3 µg/ml group, hydrogen peroxide+tribuloside 10 µg/ml group, hydrogen peroxide+microRNA-NC group, hydrogen peroxide+microRNA-335-3p group, hydrogen peroxide+tribuloside+anti-microRNA-335-3p group. Cell counting kit-8 method and flow cytometry were applied for determining cell viability and apoptosis. Malondialdehyde level, catalase and superoxide dismutase activities were determined using kits. Reverse transcription-quantitative polymerase chain reaction was used for microRNA-335-3p quantification. Kriippellike factor 6 expression was examined via Western blot. Target regulation relationship of miR-335-3p and Kriippel-like factor 6 was analyzed via dual-luciferase report assay. Contrasted with the control group, cell viability, catalase and superoxide dismutase viabilities, and microRNA-335-3p expression were significantly reduced in hydrogen peroxide group (p<0.05), while apoptosis, malondialdehyde and Kriippel-like factor 6 levels were overtly promoted (p<0.05). Contrasted to hydrogen peroxide group, cell viability, catalase and superoxide dismutase activities, and microRNA-335-3p expression in hydrogen peroxide+tribuloside 1 µg/ml group, hydrogen peroxide+tribuloside 3 µg/ml group, hydrogen peroxide+tribuloside 10 µg/ml group were obviously enhanced (p<0.05), but cell apoptosis, malondialdehyde level and Kriippel-like factor 6 protein level were suppressed (p<0.05). Relative to hydrogen peroxide+microRNA-NC group, cell viability, catalase and superoxide dismutase activities in hydrogen peroxide+microRNA-335-3p group were markedly elevated (p<0.05), whereas apoptosis inhibition, malondialdehyde level reduction and Kriippel-like factor 6 protein down-regulation were induced (p<0.05). Compared with hydrogen peroxide+tribuloside group, cell viability, catalase and superoxide dismutase activities in hydrogen peroxide+tribuloside+anti-microRNA-335-3p group were signally inhibited (p<0.05), but apoptosis, malondialdehyde and Kriippel-like factor 6 levels were accelerated (p<0.05). MicroRNA-335-3p directly interacted with Kriippel-like factor 6. Tribuloside could attenuate apoptosis and oxidative damage in hydrogen peroxide-induced cataract model, which was related to microRNA-335-3p/Kriippel-like factor 6 axis. [ABSTRACT FROM AUTHOR]

Dementia is most frequently caused by Alzheimer’s disease. The objective of this study was to investigate the potential targets of Alzheimer’s disease and its associated biological processes. We obtained gene expression profiles of the GSE5281, GSE48350 and GSE11882 datasets from the gene expression Omnibus database. Among the total datasets, 263 were of Alzheimer’s disease tissues and 204 were of healthy tissues. We selected differentially expressed genes from Alzheimer’s disease tissues and healthy tissues using the gene expression Omnibus 2R tool and Venn diagram software. Next, we used database for annotation, visualization and integrated discovery database, gene ontology database and Kyoto encyclopedia of genes and genomes pathways for analysis. Then, by using Cytoscape’s search tool for the retrieval of interacting genes, it is possible to see how these differentially expressed genes and protein-protein interactions interact with one another. In total, there were 270 consistently expressed genes, containing 193 down-regulated genes and 77 up-regulated genes. Additionally, 270 consistently expressed genes were found by chip analysis as the test set and 242 acquisitions of causative differentially expressed genes were sought via gene list automatically derived for you as the training set. ToppGene was then utilized to optimize these genes. Of the protein-protein interaction network, analysed by the molecular complex detection plugin, 14 regulated genes were selected. In conclusion, using integrated bioinformatics techniques, we have attempted to discover the substantially altered expression genes associated with a poorer prognosis in Alzheimer’s disease and the investigations may benefit their predictive and prognostic value in Alzheimer’s disease. [ABSTRACT FROM AUTHOR]