The incidence of intervertebral disc degeneration (idd) is increasing, especially among elderly individuals. The present study aimed to investigate the effects of the nF-κB/p53 signaling pathway on idd and its regulatory effect on associated cytokines. in the present study, human nucleus pulposus cells were isolated from patients with thoracic-lumbar fractures and patients with idd to observe cellular morphology and detect phosphorylated (p)-p65/p53 expression levels. The locality and expression levels of p65 in interleukin (il)-1β-stimulated nucleus pulposus cells, with or without the addition of ammonium pyrrolidinedithiocarbamate (PdTc; a nF-κB signaling pathway-specific blocker), were measured. Furthermore, the effects of il-1β stimulation on the protein and gene expression levels of idd-related cytokines were determined following p53 knockdown and inhibition of the nF-κB signaling pathway. The results suggested that p-p65 and p53 expression was significantly increased in idd cells compared with normal nucleus pulposus cells. Moreover, nucleus pulposus cells isolated from patients with idd contained less cytoplasm compared with normal nucleus pulposus cells, and p65 expression levels were higher in the cytoplasm than the nucleus of il-1β-stimulated PdTc-treated healthy nucleus pulposus cells. Moreover, the p53 expression levels were significantly decreased following transfection with sip53. PdTc treatment and p53 knockdown significantly decreased matrix metallopeptidase (MMP)-3, MMP-13, metallopeptidases with thrombospondin type 1 motif (adaMTS)-4 and adaMTS-5 expression levels, and increased aggrecan and collagen type ii expression levels in il-1β-stimulated cells. The present study indicated that activation of the nF-κB/p53 signaling pathway might be related to the occurrence of idd; therefore, the nF-κB/p53 signaling pathway may serve as a therapeutic target for idd.

Sulfide ions (S2−) that are widely distributed in biological and industrial fields are extremely toxic and pose great harms to both ecological environment and human health. However, fluorescent sensors toward S2− ions commonly use S2−-recovered fluorescence of fluorophore that is first quenched mainly by metal ions. Fluorescent probe which enables direct, selective, and sensitive detection of S2− ion is highly desirable. Herein, we demonstrate one-step preparation of fluorescent ionic liquid–graphene quantum dots (IL-GQDs) nanocomposite, which can act as a fluorescent probe for direct and sensitive detection of S2− ion. The IL-GQDs nanocomposite is easily synthesized via facile molecular fusion of carbon precursor and in situ surface modification of GQDs by IL under hydrothermal condition. The as-prepared IL-GQDs nanocomposite has uniform and ultrasmall size, high crystallinity, and bright green fluorescence (absolute photoluminescence quantum yield of 18.2%). S2− ions can strongly and selectively quench the fluorescence of IL-GQDs because of the anion exchange ability of IL. With IL-GQDs nanocomposite being fluorescent probe, direct and sensitive detection of S2− is realized with a linear detection range of 100nM–10μM and 10μM–0.2mM (limit of detection or LOD of 23nM). Detection of S2− ions in environmental river water is also achieved.

Background. A growing number of studies have suggested that microRNAs exert an essential role in the development and occurrence of multiple tumours and act as crucial regulators in various biological processes. However, the expression and function of miRNA-140 in hepatocellular carcinoma (HCC) cells are not yet adequately identified and manifested. Methods. The expression of miRNA-140 was determined in HCC tissues and adjacent nontumour tissues by quantitative real-time polymerase chain reaction (qRT-PCR). Kaplan–Meier survival analysis and Cox regression analysis were performed to explore the correlation between miRNA-140 expression level and the survival rate of patients with HCC. Additionally, overexpression experiments were conducted to investigate the biological role of miRNA-140 in HCC cells. Bioinformatics was used to predict the related target genes and pathways of miRNA-140. Results. QRT-PCR results signified that the expression level of miRNA-140 in HCC was lower than that of adjacent normal tissues ( P < 0.0001 ). Compared with the control group, the SMMC-7721 HCC cells in the miRNA-140 mimic group had a decrease in proliferation, migration, and invasion ( P < 0.05 ), whereas those in the miRNA-140 inhibitor group had an increase in proliferation, migration, and invasion ( P < 0.05 ). Cell cycle arrest occurred in the G0/1 phase. Prognosis analysis showed that the expression level of miRNA-140 was not related to the prognosis of HCC. Furthermore, the Kaplan–Meier test revealed that patients with lower miRNA-140 expression levels in liver cancer tissue had significantly shorter disease-free survival (DFS, P = 0.004 ) and overall survival (OS) times ( P = 0.010 ) after hepatectomy. Cox regression analysis further indicated that miRNA-140 was an independent risk factor that may affect the DFS ( P = 0.004 ) and OS times ( P = 0.014 ) of patients after hepatectomy. Our results suggested that miRNA-140 might be a crucial regulator involved in the HCC progression and is thus considered a potential prognostic biomarker and therapeutic target for HCC.