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Depression and anxiety amid Older folks.
Psoralen is an effective active component extracted from Psoraleacorylifolia, which can promote bone formation in osteoporotic animals. However, to the best of our knowledge, its effect on fracture healing has not yet been examined. In the present study, open femur fractures were created in ovariectomy (OVX)-induced osteoporotic mice. OVX mice were treated with psoralen (psoralen+OVX group) or physiological saline (OVX group) by oral gavage. Radiographic and histological results demonstrated progressed callus consolidation in the psoralen+OVX group compared with the OVX group after 10 and 21 days of treatment. Qualitative histological analysis showed that the number of osteoclasts was significantly reduced in the psoralen+OVX group after treatment. Moreover, reverse transcription-quantitative PCR analysis of callus samples showed increased expression of bone morphogenetic protein-2 (BMP-2) and osteoprotegerin (OPG), and decreased expression of receptor activator of nuclear factor-κB ligand (RANKL) at 10 and 21 days post injury in the psoralen+OVX group compared with the OVX group. Furthermore, western blot analysis showed that psoralen significantly increased the expression of estrogen receptor (ER)-α, but had no effect on ER-β expression; these results were further confirmed by immunohistochemistry. To conclude, these results indicated that psoralen may promote callus formation and inhibit osteoclast genesis by increasing BMP-2 and ER-α levels, and OPG/RANKL ratio. Consequently, psoralen could be a possible treatment for osteoporotic fracture-related complications.Retinoblastoma (RB) is the most common primary intraocular cancer type that occurs during retinal development in childhood. Previous studies have reported that long non-coding RNAs (lncRNAs) are involved in the development of RB. Therefore, the aim of the present study was to investigate the effects and underlying regulatory mechanisms of nuclear paraspeckle assembly transcript 1 (NEAT1) in RB. The expression levels of NEAT1, microRNA (miR)-24-3p and leucine-rich-α-2-glycoprotein (LRG1) were detected using reverse transcription-quantitative PCR (RT-qPCR). Moreover, the protein expression levels of LRG1, matrix metalloproteinase 9, N-cadherin and E-cadherin were detected via western blotting. Furthermore, cell migration and invasion abilities were evaluated via Transwell assays. The targeting relationships between miR-24-3p and NEAT1 or LRG1 were predicted using online software and confirmed via dual-luciferase reporter assay. In the present study, NEAT1 and LRG1 were upregulated, and miR-24-3p was downregulated in RB tissues and cells compared with the corresponding healthy tissues and cells. Moreover, miR-24-3p was identified as a target of NEAT and LRG1 was demonstrated to be a direct target gene of miR-24-3p. Knockdown of NEAT1 or LRG1 significantly suppressed RB cell migration and invasion ability, while the effects were reversed by an miR-24-3p inhibitor. In addition, the downregulation of LRG1 caused by miR-24-3p was restored following the overexpression of NEAT1 in RB cells. It was also demonstrated that NEAT1 knockdown inhibited the epithelial-to-mesenchymal transition (EMT) pathway by inhibiting the expression of LRG via targeting miR-24-3p. In conclusion, the present results suggest that silencing of NEAT1 suppresses cell migration, invasion and the EMT process by downregulating LRG1 expression via sponging miR-24-3p in RB, thus indicating that NEAT1 may be a potential candidate for RB treatment.Proliferation and migration of keratinocytes are major processes of skin wound repair after injury. It has been indicated that microRNAs (miRNAs/miRs) are associated with the proliferation and migration of keratinocytes. However, the mechanism by which miR-185 affects these processes in keratinocytes remains unclear. In the present study, the expression level of miR-185 and peroxisome proliferator-activated receptor β (PPARβ) was examined by reverse transcription-quantitative PCR in HaCaT keratinocytes. Cell proliferation was evaluated using Cell Counting Kit-8 and colony formation assays. Western blot analysis was used to detect the levels of cell proliferation, migration and PI3K/AKT signaling pathway-associated proteins. In addition, the migratory capacity of the cells was determined using Transwell assay. The target gene of miR-185 was verified using dual-luciferase reporter assay. The results indicated that overexpression of miR-185 inhibited proliferation, migration and activation of the PI3K/AKT signaling pathway in HaCaT keratinocytes. PPARβ was indicated to be a target of miR-185 and its overexpression promoted the proliferation and migration of HaCaT keratinocytes, while its knockdown exhibited the adverse effects. Furthermore, PI3K inhibitor LY294002 inhibited activation of the PI3K/AKT signaling pathway and decreased the proliferation and migration of HaCaT keratinocytes. In addition, overexpressed PPARβ reversed the suppressive effects of miR-185 overexpression on proliferation, migration and activation of the PI3K/AKT signaling pathway. In conclusion, the results of the present study demonstrated that miR-185 suppressed activation of the PI3K/AKT signaling pathway via targeting PPARβ, thereby regulating proliferation and migration in HaCaT keratinocytes. The present study provided a novel theoretical basis for the use of miR-185 as a target in wound repair.Knee osteoarthritis is caused by a multifactorial imbalance in the synthesis and degradation of knee chondrocytes, subchondral bone and extracellular matrix. Abnormal expression of long non-coding RNAs (lncRNAs) affects the metabolism, synovitis, autophagy and apoptosis of chondrocytes, as well as the production of cartilage matrix. The aim of the present study was to identify novel targets for the treatment of osteoarthritis and to examine the pathogenesis of the disease. Selleckchem PT2977 The lncRNA expression profiles of seven patients with knee osteoarthritis and six healthy controls were examined by RNA-sequencing. Differentially expressed lncRNAs were selected for bioinformatics analyses, including Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment. Reverse transcription-quantitative PCR (RT-qPCR) was used to further investigate the differential expression of the lncRNAs. A total of 23,583 lncRNAs were identified in osteoarthritis cartilage, including 5,255 upregulated and 5,690 downregulated lncRNAs, compared with normal cartilage.
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