Notes

Systematic applying nanoparticles throughout MALDI-MS with regard to bioanalysis.
By contrast, an inhibitor (XAV939) of Wnt/β‑catenin diminished the protective effects of hDPSC‑CM. Taken together, the findings of the present study demonstrated that the hDPSC secretome alleviated the hypoxia‑induced myoblast injury potentially through regulating the Wnt/β‑catenin pathway. These findings may provide new insight into a therapeutic alternative using the hDPSC secretome in skeletal muscle hypoxia‑related diseases.Oxidized low‑density lipoprotein (ox‑LDL)‑induced vascular endothelial damage, oxidative stress and inflammation play a vital role in the pathophysiology of atherosclerosis. Geniposide is the primary active ingredient from Gardenia jasminoides Ellis associated with anti‑oxidative properties and cardioprotective action. However, the therapeutic mechanism of geniposide in atherosclerosis remains unclear. Hence, the present study aimed to elucidate the underlying mechanisms of geniposide in oxidative stress and inflammatory response during ox‑LDL injury in human umbilical vein endothelial cells (HUVECs), focusing particularly on the microRNA (miR)‑21/PTEN pathway. The results demonstrated that geniposide pretreatment significantly increased cell viability, decreased lactate dehydrogenase release, increased miR‑21 level and decreased PTEN expression under ox‑LDL condition. Subsequently, transfection with miR‑21 mimic enhanced the protection of geniposide on ox‑LDL‑induced cytotoxicity and apoptosis (mediated by tent of the miR‑21/PTEN pathway.[Su(var)3‑9, enhancer of zeste, Trithorax] domain‑containing protein 7 (SETD7) is a protein lysine methyltransferase that methylates both histone H3K4 and non‑histone proteins, such as transcription factors. The methylation on proteins alters their activity and affects a series of biological processes. Recent studies have demonstrated that SETD7 contributes to tumor progression and may play different roles in tumor development. However, the effect of SETD7 on lung cancer cell migration and invasion has not been fully elucidated. The present study demonstrated that the expression of SETD7 was significantly downregulated in lung cancer tissues in comparison with that in matched non‑cancer tissues, and lung cancer cell lines also exhibited lower SETD7 levels compared with normal human bronchial epithelial cells. Overexpression of SETD7 inhibited the migration and invasion of lung cancer cells, whereas decreased SETD7 expression promoted cell migration and invasion. Further study revealed that SETD7 regulated the expression of the metastasis‑related genes metalloproteinase 2, Twist1 and vascular endothelial growth factor. Furthermore, SETD7 knockdown activated the Janus kinase 2/signal transducer and activator of transcription 3 (STAT3) signaling pathway and enhanced lung cancer cell migration, whereas the STAT3‑specific inhibitor Stattic abrogated the effect of SETD7 on cell migration. Taken together, these data indicated that SETD7 acts as a tumor suppressor, and the reduced expression of SETD7 may contribute to lung cancer progression. The findings of the present study suggest that SETD7 may be a novel candidate for the treatment of metastatic lung cancer.At present, the treatment of hyperuricemia is designed primarily to decrease the production of uric acid using xanthine oxidase inhibitors; however, the therapeutic effect is not satisfactory. Therefore, the key to the successful treatment of hyperuricemia is to increase the excretion of uric acid. The aim of present study was to construct uricase‑expressing genetically engineered bacteria and analyze the effects of these engineered bacteria on the lowering of uric acid levels in a rat model of hyperuricemia. The uricase expression vector was constructed by gene recombination technology and transfected into Escherichia coli. Novobiocin The expression and activity of uricase were analyzed by SDS‑PAGE analysis and Bradford assay. The water consumption, food intake, body weight, eosinophil count and intestinal histology, in addition to the levels of serum uric acid (SUA) and allantoin in the feces of the rats, were assessed. The intestinal contents of the rats were analyzed by 16S rDNA sequencing technology. The results demonstrated that uricase‑expressing genetically engineered bacteria secreted active uricase. All rats exhibited a natural growth trend during the entire experiment, and the SUA of hyperuricemic rats treated with uricase‑expressing engineered bacteria was significantly decreased. In conclusion, these results indicate that uricase secreted by recombinant uricase‑expressing genetically engineered bacteria served an important role in decreasing SUA levels in a rat model of hyperuricemia.Silibinin is a flavonoid extracted from milk thistle seeds which has been widely used as a hepatoprotective and antioxidant agent. Recently, accumulating evidence has demonstrated the anti‑cancer effects of silibinin in various cancer models. It was previously reported that silibinin induced apoptosis and decreased metastasis by activating autophagy in renal cell carcinoma (RCC). However, the underlying molecular mechanisms by which silibinin regulates autophagy remain largely unknown. The aim of the present study was to investigate the effects of silibinin on RCC metastasis in vitro and in vivo, with a focus on autophagy‑dependent Wnt/β‑catenin signaling. Human RCC 786‑O and ACHN cell lines were used as the model system in vitro and RCC xenografts of nude mice were used for in vivo studies. Silibinin inhibited metastasis and epithelial‑mesenchymal transition (EMT) of RCC in vitro and in vivo, by regulating the Wnt/β‑catenin signaling pathway. Furthermore, silibinin inhibited the Wnt/β‑catenin signaling pathway in an autophagy‑dependent manner. Autophagic degradation of β‑catenin induced by silibinin was associated with the anti‑metastatic effects of silibinin against RCC. These findings identify a novel mechanism by which silibinin inhibits EMT and metastasis of RCC, highlighting a potential novel strategy for treating metastatic RCC.Melatonin (Mel) elicits beneficial effects on myocardial ischemia/reperfusion injury. However, the underlying mechanism of Mel against oxygen‑glucose deprivation/reperfusion (OGD/R)‑induced H9c2 cardiomyocyte damage remains largely unknown. The aim of the present study was to investigate the biological roles and the potential mechanisms of Mel in OGD/R‑exposed H9c2 cardiomyocytes. The results of the present study demonstrated that Mel significantly elevated the viability and reduced the activity of lactate dehydrogenase and creatine kinase myocardial band in a dose‑ and time‑dependent manner in OGD/R‑insulted H9c2 cells. In addition, Mel suppressed OGD/R‑induced oxidative stress in H9c2 cells, as demonstrated by the decreased reactive oxygen species and malondialdehyde levels, as well as the increased activities of superoxide dismutase, catalase and glutathione peroxidase. Mel exerted an antioxidant effect by activating the peroxisome proliferator‑activated receptor gamma coactivator‑1α (PGC‑1α)/nuclear factor erythroid 2‑related factor 2 (Nrf2) signaling.
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