Notes

Very framework associated with 5-bromo-2,Four,6-trimethyl-3-[(2-methyl-phen-yl)sulfin-yl]-1-benzo-furan.
The authors' previous study demonstrated that miR‑128 may exert an inhibitory effect on the osteogenic differentiation of bone marrow‑derived mesenchymal stem cells (BM‑MSCs), but its downstream mechanisms remain to be elucidated. The aim of the present study was to investigate the microRNA (miRNA/miR) and mRNA profiles of differentiated and undifferentiated BM‑MSCs and explore new downstream targets for miR‑128. The sequencing datasets of GSE107279 (miRNA) and GSE112318 (mRNA) were downloaded from the Gene Expression Omnibus database. The differentially expressed miRNAs (DEMs) and genes (DEGs) were identified using the DESeq2 method. The target genes of DEMs were predicted by the miRwalk 2.0 database. The hub target genes of miR‑128 were screened by constructing the protein‑protein interaction (PPI) network and module analysis. The expression levels of miR‑128 and crucial target genes were validated by reverse transcription‑quantitative (RT‑q) PCR before or after transfection of miR‑128 mimics to BM‑MSCs. buy TAS4464 Thinhibit the osteoblast differentiation of BM‑MSCs by downregulation of these 6 genes, particularly RUNX1, YWHAB and NTRK2.FGD5 antisense RNA 1 (FGD5‑AS1) is a long non‑coding RNA in acute myocardial infarction (AMI), which is primarily caused by myocardial ischemia‑hypoxia. Retinoid acid receptor‑related orphan receptor α (RORA) is a key protector in maintaining heart function. However, the roles of FGD5‑AS1 and RORA in AMI have not previously been elucidated. The present study investigated the effect and mechanism of FGD5‑AS1 and RORA in human cardiomyocyte AC16 cells under hypoxia. Reverse transcription‑quantitative PCR and western blotting demonstrated that FGD5‑AS1 and RORA were downregulated in the serum of patients with AMI and hypoxia‑challenged AC16 cells. Functional experiments were performed via assays, flow cytometry and western blotting. In response to hypoxia, superoxide dismutase (SOD) activity was inhibited, but apoptosis rate and levels of reactive oxygen species and malondialdehyde were promoted in AC16 cells, accompanied by increased Bax and cleaved caspase‑3 expression levels, and decreased SOD2 and glutathione peroxidase 1 expression levels. However, hypoxia‑induced oxidative stress and apoptosis in AC16 cells were attenuated by ectopic expression of FGD5‑AS1 or RORA. Moreover, silencing RORA counteracted the suppressive role of FGD5‑AS1 overexpression in hypoxic injury. FGD5‑AS1 controlled RORA expression levels via microRNA‑195‑5p (miR‑195), as confirmed by dual‑luciferase reporter and RNA pull‑down assays. Consistently, miR‑195 knockdown suppressed hypoxia‑induced oxidative stress and apoptosis in AC16 cells, which was abrogated by downregulating FGD5‑AS1 or RORA. In conclusion, FGD5‑AS1 modulated hypoxic injury in human cardiomyocytes partially via the miR‑195/RORA axis, suggesting FGD5‑AS1 as a potential target in interfering with the progression of AMI.Viral corneal infection is a common cause of visual impairment and blindness. Polyinosinic‑polycytidylic acid, or poly(IC), is similar to viral double‑stranded RNA in structure and has been implicated in the release of a variety of cytokines, chemokines and matrix metalloproteinases (MMPs) by corneal fibroblasts. Sulforaphane (SFN) is an isothiocyanate compound found in cruciferous vegetables. The present study investigated the potential effect of SFN on the poly(IC)‑stimulated release of cytokines, chemokines and MMPs in human corneal fibroblasts (HCFs). ELISA showed that SFN was associated with a time‑ and dose‑dependent reduction in poly(IC)‑stimulated production of interleukin (IL)‑8, chemoattractant protein‑1, IL‑6, MMP‑1 and MMP‑3 by HCFs. Western blot analysis indicated that SFN suppressed the function of poly(IC) by modulating mitogen‑activated protein kinases (MAPKs), including p38 and extracellular signal‑regulated kinase (ERK), activator protein‑1 (AP‑1) component c‑Jun and the kinase, Akt, and the phosphorylation and degradation of the nuclear factor (NF)‑κB inhibitor IκB‑α. Immunofluorescence analysis revealed that SFN attenuated the production of poly(IC)‑induced nuclear translocation of the NF‑κB p65 subunit. Reverse transcription‑quantitative PCR analysis revealed that SFN prevented the poly(IC)‑induced upregulation of Toll‑like receptor 3 (TLR3) mRNA expression in HCFs. No significant cytotoxic effect of SFN on HCFs was observed. In summary, SFN attenuated the poly(IC)‑induced production of proinflammatory chemokines, cytokines and MMPs by HCFs, by inhibiting TLR3, MAPK (p38 and ERK), AP‑1, Akt and NF‑κB signaling. SFN may therefore be a potential novel treatment for viral corneal infection by limiting immune cell infiltration.After the publication of the above paper, the authors have noticed that the affiliations were presented incorrectly; essentially, Drs Rong‑qiang Yang, Peng‑fei Guo, Qing‑nan Meng, Ya Gao, Imran Khan, Xiao‑bo Wang and Zheng‑jun Cui are based at the Department of Burn and Repair Reconstruction Surgery, The First Affiliated Hospital of Zhengzhou University, whereas Drs Zhao Ma and Cheng Chang are located at The School of Basic Medical Science of Zhengzhou University. Therefore, the affiliations for this paper should have appeared as follows Rong‑Qiang Yang1, Peng‑Fei Guo1, Zhao Ma2, Cheng Chang2, Qing‑Nan Meng1, Ya Gao1, Imran Khan1, Xiao‑Bo Wang1 and Zheng‑Jun Cui1. 1Department of Burn and Repair Reconstruction Surgery, The First Affiliated Hospital of Zhengzhou University; 2The School of Basic Medical Science of Zhengzhou University, Zhengzhou, Henan 450052, P.R. China. The authors regret that these errors with the author affiliations were not noticed prior to the publication of their paper, and apologize for any inconvenience caused. [the original article was published in Molecular Medicine Reports 22 3405-3417, 2020; DOI 10.3892/mmr.2020.11413].Apigenin, an aromatic compound, exhibits antioxidant, anti‑inflammatory and anti‑viral effects. The present study aimed to investigate the effects of apigenin on cell proliferation and apoptosis of human melanoma cells A375P and A375SM. Therefore, melanoma cells were treated with apigenin to determine its anti‑proliferative and survival effects, using wound healing and MTT assays. The results revealed that melanoma cell viability was decreased in a dose‑dependent manner. Furthermore, chromatin condensation, indicating apoptosis, was significantly increased in a dose‑dependent manner, as demonstrated by DAPI staining. In addition, increased apoptosis rate following treatment with apigenin was confirmed by Annexin V‑propidium iodide staining. The changes in the expression levels of apoptosis‑related proteins in A375P and A375SM melanoma cells were subsequently detected using western blot analysis. The results demonstrated that the protein expression levels of Bcl‑2 were decreased, whereas those of Bax, cleaved poly ADP‑ribose polymerase, cleaved caspase‑9 and p53 were upregulated in a dose‑dependent manner in apigenin‑treated cells compared with those noted in untreated cells.
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