Aberrant proliferation and apoptosis of vascular smooth muscle cells (VSMCs) serve a dominant role in the pathogenesis of atherosclerosis (AS). Long non‑coding (lnc)RNA H19 is reported to accelerate the progression of AS by inhibiting the apoptosis of VSMCs, whereas p53 is identified as promoting VSMC apoptosis. The present study aimed to explore the effects of H19/p53 on the pathogenesis of AS. Apolipoprotein E knockout (ApoE‑/‑) mice fed a high‑fat diet were used as in vivo AS models. Reverse transcription‑quantitative PCR and western blot were used to detect mRNA and protein expression levels, respectively. VSMC proliferation and apoptosis were respectively assessed by CCK‑8 and flow cytometry. Compared with the control group, mouse weight and plaque area were all increased in the AS model group, as was the expression of H19. Knockdown of H19 reduced the proliferation and induced apoptosis of VSMCs, and increased the expression of p53, cleaved caspase3 (c‑caspase3) and p53 upregulated modulator of apoptosis, as well as enhancing the interaction between Bax and p53 proteins. Downregulation of H19 reduced the plaque area and promoted the expression of c‑caspase3 in mouse aortic tissues in vivo, as well as enhancing the effects of simvastatin, a drug used for AS treatment. Results from the present study indicated that knockdown of H19 may prevent AS deterioration through increased p53‑mediated VSMC apoptosis.An orally bioavailable small molecule inhibitor of plasminogen activator inhibitor‑1 (PAI‑1) is currently being clinically assessed as a novel antithrombotic agent. Although PAI‑1 is known to serve a key role in the pathogenesis of metabolic syndrome (MetS) including nonalcoholic steatohepatitis (NASH), the pharmacological action of an oral PAI‑1 inhibitor against the development of MetS‑related liver fibrosis remains unclear. The current study was designed to explicate the effect of TM5275, an oral PAI‑1 inhibitor, on MetS‑related hepatic fibrogenesis. The in vivo antifibrotic effect of orally administered TM5275 was investigated in two different rat MetS models. Fischer 344 rats received a choline‑deficient L‑amino‑acid‑defined diet for 12 weeks to induce steatohepatitis with development of severe hepatic fibrosis. Otsuka Long‑Evans Tokushima Fatty rats, used to model congenital diabetes, underwent intraperitoneal injection of porcine serum for 6 weeks to induce hepatic fibrosis under diabetic conditions. In each experimental model, TM5275 markedly ameliorated the development of hepatic fibrosis and suppressed the proliferation of activated hepatic stellate cells (HSCs). Additionally, the hepatic production of tumor growth factor (TGF)‑β1 and total collagen was suppressed. In vitro assays revealed that TGF‑β1 stimulated the upregulation of Serpine1 mRNA expression, which was inhibited by TM5275 treatment in cultured HSC‑T6 cells, a rat HSC cell line. Furthermore, TM5275 substantially attenuated the TGF‑β1‑stimulated proliferative and fibrogenic activity of HSCs by inhibiting AKT phosphorylation. Collectively, TM5275 demonstrated an antifibrotic effect on liver fibrosis in different rat MetS models, suppressing TGF‑β1‑induced HSC proliferation and collagen synthesis. Thus, PAI‑1 inhibitors may serve as effective future therapeutic agents against NASH‑based hepatic fibrosis.Acute lung injury (ALI) is a complex condition frequently encountered in the clinical setting. The aim of the present study was to investigate the effect of conditioned media (CM) from human adipose‑derived mesenchymal stromal cells (MSCs) activated by flagellin (F‑CM), a Toll‑like receptor 5 ligand, on inflammation‑induced lung injury. In the in vitro study, RAW264.7 macrophages treated with F‑CM had a higher proportion of cells with the M2 phenotype, lower expression of pro‑inflammatory factors and stronger expression of anti‑inflammatory genes compared with the CM from normal adipose‑derived MSCs. Furthermore, in vivo experiments were performed in mice with ALI induced by intraperitoneal injection of lipopolysaccharide. F‑CM significantly alleviated the lung exudation, inhibited inflammatory cell recruitment in lung tissues and decreased the concentration of inflammatory factors in the bronchoalveolar lavage fluid. These findings indicated that F‑CM has superior anti‑inflammation ability compared with CM, and that it may represent a promising therapeutic approach to the treatment of inflammation‑induced ALI.The association of the peripheral lymphocyte‑to‑monocyte ratio (LMR) with α‑fetoprotein (AFP) status in patients with AFP‑positive and AFP‑negative hepatocellular carcinoma (HCC) has not been investigated in detail. The aim of the present study was to examine the association between the LMR and AFP status in these patients. The samples were obtained from patients with a hepatitis B virus (HBV) infection, who were negative for non‑HBV hepatitis viruses and who did not suffer from autoimmune hepatitis. These patients were retrospectively reviewed and the differences of test indicators in the AFP‑negative and AFP‑positive groups were assessed. Flow cytometry was used to detect the expression levels of CD4, CD8 and programmed cell death protein 1 (PD‑1), and ELISAs were used to analyze the expression levels of interleukin (IL)‑10 and transforming growth factor (TGF)‑β1. In addition, luciferase reporter assays were used to assess binding of the IL‑10 promoter to the glucocorticoid receptor (GR) gene. Receiver operive of low AFP expression in HBV‑associated HCC patients.Lung cancer is a common malignant disease with a high incidence rate worldwide, posing a great threat to human health. To date, only a small number of studies have assessed the potential anti‑cancer effect of artesunate (Art) and the associated mechanisms in lung cancer. The present study aimed to investigate the inhibitory effects of Art in human lung cancer cells and investigated the underlying molecular mechanisms. The inhibitory effect of Art on the growth of A549 lung cancer cells was detected by the MTT assay, and flow cytometry was utilized to determine cell cycle progression, apoptosis, mitochondrial membrane potential, as well as the expression of Bcl‑2 and Bax proteins in A549 cells after Art treatment for 24 h. Art inhibited the growth of A549 cells in a dose‑dependent manner, induced cell apoptosis and cell cycle arrest, decreased the expression of Bcl‑2 protein and mitochondrial membrane potential, and increased the expression of Bax protein. In conclusion, Art significantly inhibited the growth of lung cancer cells by preventing cell cycle progression. This phenomenon indicated its promising therapeutic potential in the treatment of lung cancer.Hydrogen exhibits therapeutic and preventive effects against various diseases. The present study investigated the potential protective effect and dose‑dependent manner of hydrogen inhalation on high fat and fructose diet (HFFD)‑induced nonalcoholic fatty liver disease (NAFLD) in Sprague‑Dawley rats. Rats were randomly divided into four groups i) Control group, regular diet/air inhalation; ii) model group, HFFD/air inhalation; iii) low hydrogen group, HFFD/4% hydrogen inhalation; and iv) high hydrogen group, HFFD/67% hydrogen inhalation. After a 10‑week experiment, hydrogen inhalation ameliorated weight gain, abdominal fat index, liver index and body mass index of rats fed with HFFD and lowered the total area under the curve in an oral glucose tolerance test. Hydrogen inhalation also ameliorated the increase in liver lipid content and alanine transaminase and aspartate transaminase activities. Liver histopathologic changes evaluated with hematoxylin and eosin as well as Oil Red O staining revealed lower lipid deposition in hydrogen inhalation groups, consistent with the decrease in the expression of the lipid synthesis gene SREBP‑1c. The majority of the indicators were affected following treatment with hydrogen in a dose‑dependent manner. In conclusion, hydrogen inhalation may play a protective role by influencing the general state, lipid metabolism parameters, liver histology and liver function indicators in the rat model of metabolic syndrome with NAFLD.Peripheral blood mononuclear cells (PBMCs) contribute to the deposition of immunoglobulin A (IgA) and progression of IgA nephropathy (IgAN). This study was performed to identify novel microRNAs (miRNAs/miRs) associated with IgAN. Small RNAs were isolated from PBMCs collected from 10 healthy participants and 10 patients with IgAN; the RNAs were then subjected to high‑throughput small RNA sequencing. The results showed that miRNAs constituted 70.33 and 69.83% of small RNAs in PBMCs from healthy participants and patients with IgAN, respectively. In total, 44 differentially expressed miRNAs were identified, of which 34 were upregulated and 10 were downregulated. Among these differentially expressed miRNAs, most showed novel associations with IgAN, except miR‑148a‑3p, miR‑184 and miR‑200a. Furthermore, Kyoto Encyclopedia of Genes and Genomes pathway analysis revealed that the target genes of the differentially expressed miRNAs were primarily enriched in cancer pathways, the PI3K‑Akt signaling pathway and MAPK pathways, all of which control cell proliferation and gene expression. Moreover, miR‑3121‑3p, miR‑203a‑3p and miR‑200a‑3p may regulate core 1 synthase, glycoprotein‑N‑acetylgalactosamine 3‑β‑galactosyltransferase 1 (C1GALT1) expression by binding to its 3′ untranslated region. In conclusion, 44 differentially expressed miRNAs were discovered, 41 of which were newly found to be associated with IgAN. The differentially expressed miRNAs may regulate the progression of IgAN by controlling the behavior of PBMCs or deposition of IgA via targeting of signaling pathways or expression of C1GALT1. These findings may provide a basis for further research regarding IgAN diagnosis and therapy.Mitogen‑activated protein kinase (MAPK) signal transduction pathways may be involved in the destruction of pancreatic islet β cells induced by inflammatory cytokines. The present study aimed to investigate the role of different MAPK signal transduction pathways in the interleukin‑1β (IL‑1β)‑induced inhibition of glucose‑stimulated insulin secretion (GSIS) in Min6 mouse pancreatic cells. Min6 cells were stimulated with different concentrations of glucose (0.0, 5.5, 11.1 and 22.2 mmol/l), or different concentrations of IL‑1β (0.00, 0.25 and 2.50 ng/ml) in combination with high glucose (22.2 mmol/l) and the culture supernatant was collected. The concentration of insulin was measured by enzyme‑linked immunosorbent assay and the activation of different MAPK pathways was assessed by measuring the phosphorylation levels of extracellular signal‑regulated kinase 1/2 (ERK1/2), p38 and c‑jun N‑terminal kinase (JNK) via western blotting. The production of reactive oxygen species (ROS) was determined via flow cytometry, and cell viability was detected by Cell Counting Kit‑8 assay. Reverse transcription‑quantitative PCR was used to detect the insulin 1 gene. The results revealed that glucose activated ERK1/2 phosphorylation, but inhibited JNK and p38 phosphorylation in a concentration‑dependent manner. Furthermore, IL‑1β inhibited glucose‑stimulated insulin secretion in a dose‑dependent manner. Western blotting revealed that IL‑1β inhibited the activation of ERK1/2 phosphorylation and attenuated the inhibition of p38 phosphorylation induced by glucose stimulation. JNK was neither activated nor inhibited by IL‑1β. These results suggest that MAPK signal transduction pathways participated in the IL‑1β‑induced GSIS inhibition in Min6 cells, with the ERK1/2, JNK and p38 signaling pathways playing different roles.