Rheumatoid arthritis (RA) is an autoimmune disease of unknown etiology, which occurs in ~1.0% of the general population. Increasing studies have suggested that long non-coding RNAs (lncRNAs) may serve important roles in various biological processes and may be associated with the pathogenesis of different types of disease, including RA. Astragalosides (AST) has been used as a traditional Chinese medicine for the treatment of RA. However, the mechanism underlying its therapeutic effect has remained unclear to date. Thus, there is an urgent need to elucidate the possible mechanism of AST in the treatment of RA from the perspective of lncRNAs. In the present study, the lncRNAs and mRNAs of a vehicle group, animal model group and AST treatment (control) group were determined by Arraystar Rat lncRNA/mRNA microarray. The differentially expressed genes with a fold change >1.5 and P<0.05 were selected and analyzed. Gene Ontology (GO) and pathway analysis was performed using the Database for Annotation, Visualization and Integration Discovery, and the coding-non-coding gene co-expression network was drawn based on the correlation analysis between the differentially expressed lncRNAs and mRNAs. Based on node degree and the correlation between bioinformatics analysis and RA, the critical differentially expressed lncRNAs were selected, analyzed and verified by reverse transcription-quantitative PCR (RT-qPCR) analysis. The results showed that, following AST treatment, up to 75 lncRNAs and 247 mRNAs were found to be differentially expressed among the three groups. GO and pathway analysis manifested that 135 GO terms and 17 pathways were enriched by differentially expressed genes. Four lncRNAs (MRAK012530, MRAK132628, MRAK003448 and XR_006457) were selected as the critical lncRNAs and their trend in expression showed consistency between the RT-qPCR and microarray data. In conclusion, AST had a regulatory effect on differentially expressed lncRNAs during the development of RA, and four lncRNAs could be selected as critical therapeutic targets of AST.
Background. Type 2 diabetes mellitus (T2DM) has become a chronic disease, serious harm to human health. Complications of the blood pipe are the main cause of disability and death in diabetic patients, including vascular lesions that directly affects the prognosis of patients with diabetes and survival. This study was to determine the influence of high glucose and related mechanism of vascular lesion of type 2 diabetes mellitus pathogenesis. Methods. In vivo aorta abdominalis of GK rats was observed with blood pressure, heart rate, hematoxylin and eosin (H&E), Masson, and Verhoeff staining. In vitro cells were cultured with 30 mM glucose for 24 h. RT-QPCR was used to detect the mRNA expression of endothelial markers PTEN, PI3K, Akt, and VEGF. Immunofluorescence staining was used to detect the expression of PTEN, PI3K, Akt, and VEGF. PI3K and Akt phosphorylation levels were detected by Western blot analysis. Results. Heart rate, systolic blood pressure, diastolic blood pressure, and mean blood pressure in the GK control group were higher compared with the Wistar control group and no difference compared with the GK experimental model group. Fluorescence intensity of VEGF, Akt, and PI3K in the high-sugar stimulus group was stronger than the control group; PTEN in the high-sugar stimulus group was weakening than the control group. VEGF, Akt, and PI3K mRNA in the high-sugar stimulus group were higher than the control group; protein expressions of VEGF, Akt, and PI3K in the high-sugar stimulus group were higher than the control group. PTEN mRNA in the high-sugar stimulus group was lower than the control group. Protein expression of PTEN in the high-sugar stimulus group was lower than the control group. Conclusions. Angiogenesis is an important pathogenesis of T2DM vascular disease, and PTEN plays a negative regulatory role in the development of new blood vessels and can inhibit the PI3K/Akt signaling pathway.
asthma, a common but poorly controlled disease, is one of the most serious health problems worldwide; however, the mechanisms underlying the development of asthma remain unknown. long non-coding rnas (lncrnas) and mrnas serve important roles in the initiation and progression of various diseases. The present study aimed to investigate the role of differentially expressed lncrnas and mrnas associated with asthma. differentially expressed lncrnas and mrnas were screened between the expression data of 62 patients with asthma and 43 healthy controls. Gene ontology (Go) and Kyoto encyclopedia of Genes and Genomes (KeGG) analyses were performed to investigate the biological functions and pathways associated with the lncrnas and mRNAs identified. Protein-protein interaction (PPI) networks were subsequently generated. in addition, lncrna-mrna weighted co-expression networks were obtained. in total, 159 differentially expressed lncrnas and 1,261 mrnas were identified. GO and KEGG analyses revealed that differentially expressed mrnas regulated asthma by participating in the 'vascular endothelial (VeGF) signaling pathway', 'oxidative phosphorylation', 'Fc ε ri signaling pathway', 'amino sugar and nucleotide sugar metabolism', 'histidine metabolism', 'β-alanine metabolism' and 'extracellular matrix-receptor interaction' (P<0.05). Furthermore, protein kinase B 1 had the highest connectivity degree in the PPi network, and was significantly enriched in the 'VEGF signaling pathway' and 'Fc ε ri signaling pathway'. a total of 8 lncrnas in the lncrna-mrna co-expression network were reported to interact with 52 differentially expressed genes, which were enriched in asthma-associated Go and KeGG pathways. The results obtained in the present study may provide insight into the profile of differentially expressed lncrnas associated with asthma. The identification of a cluster of dysregulated lncrnas and mrnas may serve as a potential therapeutic strategy to reverse the progression of asthma.
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