Crabtreehenningsen8607

The liver is an important organ for the removal of toxins and utilization of nutrients. The present study then investigated whether a mixture of mulberry water extracts and silk amino acids protected against acute liver damage in rats induced by intraperitoneal injection of D-galactosamine and the action mechanism. Trastuzumab deruxtecan D-galactosamine injection is widely used to develop experimental animal models of acute hepatic disease. In the present study, male Sprague-Dawley rats received intraperitoneal injection of D-galactosamine followed by 200 and 600 mg/kg body weight (BW) of mulberry extracts and silk amino acids (13, w/w; MS13-L and MS13-H), the same amounts of MS with different ratios (15, w/w; MS15-L and MS15-H), and 600 mg/kg bw cellulose (control) for 1 week. The normal-control group received an injection of saline instead of D-galactosamine with the same diet as the control group. D-galactosamine injection (control rats) increased serum ALT, AST and γ-GPT levels, indicating the induction of acute liver damage. The control rats also exhibited reduced glycogen depositions, which contributed to increasing fat synthesis from glucose and elevated serum triglyceride levels. Oxidative stress and inflammation in the liver of the control increased in response to the decreasing antioxidant activity and mRNA expression and increasing TNF-α expression, respectively. Both MS13 and MS15 reduced serum ALT, AST and γ-GPT levels to ameliorate liver damage. MS13 reduced oxidative stress by increasing the activity and expression of antioxidant enzymes, whereas MS15 decreased the expression TNF-α in the liver. MS13 and MS15 improved the necrosis of hepatocytes in H&E staining, which was associated with increased glycogen deposition in PAS staining. MS15 had better effects on glycogen accumulation. In conclusion, MS13 and MS15 can be used as therapeutic agents for acute liver damage. Copyright © Park et al.MicroRNA-454 (miR-454), is involved in the progression of various types of cancers. The present study aimed to evaluate the effect of miR-454 on the progression of gastric cancer. SGC-7901 cells overexpressing or silencing miR454 were constructed via transfection and the survival rate of the cells was determined. The relationship between miR-454 and cylindromatosis (CYLD) was explored and the influence of miR-454 on oxaliplatin resistance was investigated in SGC-7901 cells. It was determined that overexpression of miR-454 increased the number of colonies and reduced apoptosis rate of SGC-7901 cells. The CYLD gene was identified as a direct target of miR-454. miR-454 overexpression downregulated the expression of CYLD, leading to an increase in SGC-7901 cell proliferation. Finally, miR-454 was also demonstrated to induce resistance to oxaliplatin in gastric cancer cells. In conclusion, the present in vitro findings suggested that miR-454 might be a novel therapeutic target for gastric cancer. Copyright © Huang et al.Recurrent upper gastrointestinal (UGI) and cardiovascular (CV) events of the three antiplatelet therapies in patients with cardiovascular diseases (CVD) were compared. Studies published in the PubMed, Embase, and Cochrane Central Register of Controlled Trials electronic databases that compared differences in adverse outcomes associated with the three antiplatelet therapies were reviewed. Five studies with a total number of 7,399 patients were included. No significant differences were found in the incidence of recurrent UGI events among the three antiplatelet therapies. However, in the aspirin-induced ulcer bleeding subgroups, aspirin plus proton pump inhibitors (PPIs) was associated with a significantly lower risk of recurrent UGI events (OR 0.06, 95% CI 0.01-0.32; z=3.30 and P=0.001) and UGI bleeding (OR 0.06, 95% CI 0.01-0.34; z=3.24 and P=0.001) compared to clopidogrel alone. Both aspirin plus PPIs (OR 2.12, 95% CI 1.58-2.84; z=5.00 and P less then 0.01) and clopidogrel plus PPIs (OR 2.57, 95% CI 1.89-3.51; z=5.97 and P less then 0.01) were related to a comparatively higher risk of recurrent CV events when compared to clopidogrel alone. In patients at high UGI bleeding risk (regardless of whether it was aspirin-induced) and under treatment of single antiplatelet therapy, aspirin plus PPIs should be considered as the first choice for UGI protection rather than clopidogrel alone and clopidogrel plus PPIs. However, in terms of CV protection, clopidogrel alone appears to be superior in reducing CV risk, while clopidogrel plus PPIs may relate to an increased CV risk due to the potential drug-drug interaction. Copyright © Wu et al.Function of long non-coding RNA urothelial carcinoma antigen 1 (lncRNA UCA1) in regulating the proliferative and migratory abilities of vascular smooth muscle cells (VSMCs) by mediating matrix metalloproteinase-9 (MMP9) level were elucidated. After treatment with different concentrations of ox-LDL for different time points, lncRNA UCA1 level in VSMCs was determined by quantitative real-time polymerase chain reaction (qRT-PCR). Subcellular distribution of UCA1 was analyzed. Proliferative and migratory abilities of VSMCs transfected with pcDNA-UCA1 were assessed. Protein level of MMP9 in HA-VSMCs treated with different concentrations of ox-LDL for different time points was also determined. The potential interaction between UCA1 and enhancer of zeste homolog 2 (EZH2) was identified by RNA immunoprecipitation (RIP) assay. Recruitment ability of EZH2 to MMP9 promoter region influenced by UCA1 was determined by Chromatin immunoprecipitation (ChIP) assay. Finally, the potential function of MMP9 in UCA1-mediated cellular behavior of VSMCs was explored. UCA1 was time-dependently and dose-dependently upregulated in VSMCs by ox-LDL treatment. Proliferative and migratory abilities of VSMCs were enhanced by treatment of 100 mg/l ox-LDL for 48 h, which were further reduced after transfection of pcDNA-UCA1. Subcellular distribution analysis showed that UCA1 was mainly distributed in the nucleus. Protein level of MMP9 was gradually elevated with the treatment of increased concentrations of ox-LDL in VSMCs. Its level was downregulated by transfection of pcDNA-UCA1 in VSMCs. The interaction between UCA1 and EZH2 was confirmed by RIP assay. Transfection of pcDNA-UCA1 stimulated the binding of EZH2 on MMP9 promoter region. Finally, overexpression of MMP9 reversed the decreased proliferative and migratory abilities in ox-LDL-treated VSMCs overexpressing UCA1. Downregulated UCA1 accelerates VSMCs to proliferate and migrate through negatively regulating MMP9 level. Copyright © Xu et al.