Additionally, FGF2 was shown to be a target of miR-424-5p, which in turn, was a target of SNHG1. miR-424-5p silencing and FGF2 overexpression both reversed the suppressive effects of SNHG1 knockdown on the proliferation, migration and invasion of OS cells. Thus, the silencing of SNHG1 may inhibit the proliferation, migration and invasion of OS cells by regulating the miR-424-5p/FGF2 axis.Acute pancreatitis (AP) is a common gastrointestinal disease that can become severe, so that intensive care may be required. This study was to examine serum soluble intercellular adhesion molecule-1 (sICAM-1), and soluble receptor for advanced glycation end products (sRAGE) for efficacy and prognosis prediction of glutamine (Glu) combined with ulinastatin (UTI) on severe acute pancreatitis (SAP). Fifty-four mild acute pancreatitis (MAP) patients admitted to Yidu Central Hospital of Weifang were selected as the MAP group (MAPG), 80 with SAP were divided as the SAP group (SAPG), and 60 healthy individuals who came to Yidu Central Hospital of Weifang for physical examination during the same period were included to the normal group (NG). Serum sICAM-1 and sRAGE were measured and their predictive value of efficacy and prognosis were analyzed. In view of the treatment effectiveness and prognosis, the patients were divided into effective group (EG) and ineffective group (IG), good prognosis group (GPG) and poor prognosis group (PPG). The levels of D-lactate, diamine oxidase (DAO), endotoxin and T-lymphocyte subsets (CD3+, CD4+, CD8+ and CD4+/CD8+) were measured and the changes before and after treatment were analyzed. The AUC values of NG and MAPG, NG and SAPG, MAPG and SAPG were 0.857, 0.939 and 0.856, respectively, those of predicting efficacy were 0.920 and 0.874, respectively, and those of poor prognosis in the SAPG were 0.914 and 0.879, respectively. In the SAPG, D-lactate, DAO, endotoxin and CD8+ decreased markedly after treatment, but CD3+, CD4+, and CD4+/CD8+ were opposite. SICAM-1 and sRAGE were also independent risk factors for poor prognosis in the SAPG. Serum sICAM-1 and sRAGE have high predictive value for early diagnosis, efficacy and prognosis of Glu combined with UTI.Endothelial-cell (EC) apoptosis serves a vital role in the pathogenesis of atherosclerosis. Accumulating evidence has implicated microRNA (miRNA/miR) dysregulation in EC apoptosis. Although the role of miR-454-3p in carcinogenesis has been well documented, its role and underlying mechanism in EC apoptosis remain unclear. In the present study, the results revealed that miR-454-3p expression was substantially downregulated in human aortic endothelial cells (HAECs) following oxidized low-density lipoprotein (ox-LDL) treatment. miR-454-3p suppression significantly attenuated the viability of HAECs, while miR-454-3p overexpression repressed ox-LDL-induced HAEC apoptosis. Bioinformatics analysis and luciferase reporter assays revealed that transient receptor potential canonical 3 (TRPC3), a key regulator of atherosclerosis development, was the direct target of miR-454-3p. Furthermore, TRPC3 overexpression abolished the anti-apoptotic effect of miR-454-3p on HAECs. These results revealed a novel role of miR-454-3p in ox-LDL-induced apoptosis in HAECs.Benign prostatic hyperplasia (BPH) with lower urinary tract symptoms (LUTS) is a common disease among elderly men, for which safe and effective treatment strategies remain limited. The aim of the present study was to explore the potential effects of phosphodiesterase 5A3 (PDE5A3) silencing on human prostate smooth muscle cells (HPSMCs). HPSMCs were initially obtained from patients with BPH/LUTS. Short hairpin RNA (shRNA) targeting the PDE5A3 gene was subsequently transfected into cultured HPSMCs. The expression of PDE5A3 was measured using reverse transcription-quantitative PCR and western blotting. cGMP levels were then measured using western blotting and immunocytochemical staining and intracellular Ca2+ concentration was measured using rhod2-AM in HPSMCs after transfection. HPSMC proliferation was also observed within 4 days. Cells transfected with PDE5A3-shRNA2 exhibited the most notable decline in PDE5A3 expression compared with that in the Control or NC groups. cGMP levels in HPSMCs transfected with PDE5A3-shRNA2 was significantly increased compared with those in the Control or NC groups, whereas intracellular Ca2+ concentrations in cells in the PDE5A3-shRNA2 group were decreased compared with that in the Control or NC groups. this website The proliferation of HPSMCs in the PDE5A3-shRNA2 group was also inhibited compared with that in the Control or NC groups after 72 h of culture. In conclusion, shRNA-mediated silencing of PDE5A3 was able to increase the levels of cGMP whilst reducing the concentration of Ca2+ in HPSMCs, in turn suppressing their proliferation. These findings may potentially provide a novel therapeutic target for treating BPH/LUTS.Neutrophil gelatinase-associated lipocalin (NGAL), also called lipocalin 2, is considered a promising biomarker for acute and chronic kidney injuries. Several studies have demonstrated that its levels increase in plasma and urine in diabetic nephropathy (DN), and its urine concentration increases upon kidney function deterioration. However, its role in DN progression remains unclear. The current study used in vitro gene expression knockdown in human proximal tubular cell line human kidney (HK)2 to investigate the role of NGAL in oxidation and extracellular matrix secretion under high-glucose (HG) incubation. In addition, type 1 diabetes was induced in vivo in knockout NGAL-/- and wild-type mice in order to investigate role of NGAL in the progression of DN. The results demonstrated that NGAL knockdown in HK2 cells significantly increased oxidative stress under HG stimulation tested by flow cytometry, and increased the secretion of interleukin-6, fibronectin (FN) and collagen IV examined by ELISA. Western blotting demonstrated that the phosphorylation of Smad2/3 also increased in HK2 cells under transforming growth factor-β1 stimulation. In vivo experiments demonstrated that diabetic NGAL-/- mice showed deteriorated renal function compared with that of diabetic wild-type mice. Histopathological analysis suggests that diabetic NGAL-/- mice had more serious glomerulosclerosis and tubular vascular degeneration than wild-type mice. Immunohistochemistry suggested that the absence of NGAL lead to increased FN deposition in glomeruli in a mouse model of DN. In conclusion, NGAL appears to have renal protective effects by slowing down the progression of DN, and its effect may be associated with a reduction in oxidation, fibrosis and inflammation.