Silibinin is a flavonoid that improves fatty liver and insulin resistance. To elucidate the effect of silibinin on lipid deposition and the potential molecular mechanism, the present study conducted in vivo and in vitro experiments. In the in vivo experiments, mice were randomly divided into control, high‑fat and silibinin groups, while HepG2 cells were randomly divided into control, palmitic acid intervention and silibinin intervention groups. The mRNA, protein and miR‑122 expression associated with hepatic lipid metabolism were detected in each group. The results demonstrated that silibinin reduced the triglyceride content, miR‑122 expression and the mRNA and protein expressions of fatty acid synthase (FAS) and acetyl‑CoA carboxylase (ACC). Silibinin increased the mRNA and protein expression of carnitine palmitoyl transferase 1A (CPT1A). In the present study, HepG2 cells cultured with palmitate were treated with silibinin following overexpression of micro RNA (miR) 122. The results demonstrated that the mRNA and protein expression of FAS and ACC was increased, while that of CPT1A was decreased. Therefore, it could be deduced that silibinin improved lipid metabolism by reducing the expression of miR‑122 and inhibiting the expression of miR‑122 may be a new therapeutic target to improve fatty liver disease.Programmed cell death protein‑1 (PD‑1)/programmed death protein ligand‑1 (PD‑L1) inhibitors for treatment of a various types of cancers have revolutionized cancer immunotherapy. However, PD‑1/PD‑L1 inhibitors are associated with a low response rate and are only effective on a small number of patients with cancer. Development of an anti‑PD‑1/PD‑L1 sensitizer for improving response rate and effectiveness of immunotherapy is a challenge. The present study reviews the synergistic effects of PD‑1/PD‑L1 inhibitor with oncolytic virus, tumor vaccine, molecular targeted drugs, immunotherapy, chemotherapy, radiotherapy, intestinal flora and traditional Chinese medicine, to provide information for development of effective combination therapies.Tumors of the abdominal cavity, such as colorectal, pancreatic and ovarian cancer, frequently metastasize into the peritoneum. Large numbers of metastatic nodules hinder curative surgical resection, necessitating lavage with hyperthermic intraperitoneal chemotherapy (HIPEC). However, HIPEC not only causes severe side effects but also has limited therapeutic efficacy in various instances. At the same time, the age of immunotherapies such as biological agents, checkpoint‑ inhibitors or immune‑cell therapies, increasingly emphasizes the critical role of anticancer immunity in targeting malignancies. The present study investigated the ability of three types of long‑lived reactive species (oxidants) to inactivate cancer cells and potentially complement current HIPEC regimens, as well as to increase tumor cell expression of danger signals that stimulate innate immunity. The human abdominal cancer cell lines HT‑29, Panc‑01 and SK‑OV‑3 were exposed to different concentrations of hydrogen peroxide (H2O2), hypochlorous targeting peritoneal carcinomatosis.Hepatocellular carcinoma (HCC) is a malignant tumor located in the liver. Secreted frizzled‑related protein 4 (sFRP‑4) is associated with cancer occurrence, but the relationship between sFRP‑4 and HCC is not completely understood. The present study aimed to investigate the role and mechanism underlying sFRP‑4 in HCC. sFRP‑4 mRNA expression levels were determined via reverse transcription‑quantitative PCR and immunohistochemistry. The Cell Counting Kit‑8 assay was performed to evaluate HCCLM3 and Huh7 cell viability. Moreover, HCCLM3 and Huh7 cell proliferation were assessed using the BrdU ELISA assay kit, and cell apoptosis was measured via flow cytometry. Western blotting was conducted to measure β‑catenin and GSK‑3β protein expression levels. The results demonstrated that sFRP‑4 expression was significantly downregulated in HCC tissues and cells compared with adjacent healthy tissues and MIHA cells, respectively. Moreover, the results indicated that compared with the control group, sFRP‑4 overexpression inhibited HCC cell viability and proliferation, and accelerated HCC cell apoptosis. Furthermore, the results suggested that sFRP‑4 inhibited the Wnt/β‑catenin signaling pathway by upregulating GSK‑3β expression and downregulating β‑catenin expression, thus restraining the malignant behavior of HCC cells. In conclusion, the present study indicated that sFRP‑4 served a tumor suppressor role in HCC cells by restraining the Wnt/β‑catenin signaling pathway.Intestinal inflammation frequently occurs alongside dysmotility, which is characterized by altered myosin light chain phosphorylation levels. Curcumin, an active component from the ginger family, is reported to confer anti‑inflammatory effects. However, the effects of curcumin on both diarrhea and constipation associated inflammation remains to be elucidated. The present study was designed to investigate the effects of curcumin on diarrhea and constipation and to determine the related mechanisms. Sprague‑Dawley rats were used to establish diarrhea and constipation models via intracolonic acetic acid (4%) instillation or cold water gavage for 2 weeks, respectively. Blood samples were collected to measure the serum levels of the cytokines TNF‑α and IL‑1β using ELISA kits. Western blotting was performed to measure NF‑κB, RhoA, Rho‑related kinase 2, phosphorylated MLC20, phosphorylated myosin phosphorylated target subunit 1, 130k Da‑MLC kinase (MLCK), c‑kit tyrosine kinase protein expression, and reverse transcriarrhea and constipation, were explored in the present study. Results from the present study suggested that curcumin has potential therapeutic value for treating intestinal inflammation and inflammation‑related motility disorders.It has previously been shown that the number of endothelial progenitor cells (EPCs) is negatively correlated with Syntax score in patients with coronary artery disease (CAD). However, the association between alterations in EPC function and Syntax score is still unknown. The present study evaluated the association between the activity of EPCs as well as endothelial function and Syntax score in patients with CAD and investigated the underlying mechanisms. A total of 60 patients with CAD were enrolled in 3 groups according to Syntax score, and 20 healthy subjects were recruited as the control group. selleck chemical The number and migratory, proliferative and adhesive activities of circulating EPCs were studied. The endothelial function was measured by flow‑mediated dilatation (FMD) and the levels of nitric oxide (NO) in plasma or secreted by EPCs were detected. The number and activity of circulating EPCs were lower in patients with a high Syntax score, which was similar to the alteration in FMD. The level of NO in plasma or secreted by EPCs also decreased as Syntax score increased.