MicroRNA-509-3p Inhibits Cancer Cell Proliferation and Migration via Upregulation of XIAP in Gastric Cancer Cells.

Gastric cancer (GC) is the fourth most common cancer globally. Recently, microRNAs (miRNAs) have been suggested to be closely associated with tumorigenesis. Aberrant expression of miR-509-3p has been reported in cancer studies. However, the expression and mechanism of its function in GC remain unclear. Here we showed that miR-509-3p was downregulated in GC specimens, which was associated with overall survival. Functional investigations demonstrated that the overexpression of miR-509-3p inhibited the migration and proliferation of the GC cells. Additionally, we identified X-linked inhibitor of apoptosis protein (XIAP) as a direct target of miR-509-3p. Knockdown of XIAP significantly attenuated the ability of proliferation, migration, and invasion of GC cells. The data therefore suggest that miR-509-3p plays an important role in the development and progression of GC, implicating possible applications in the clinic as a biomarker and a potential new target.

Baicalin ameliorates isoproterenol-induced acute myocardial infarction through iNOS, inflammation, oxidative stress and P38MAPK pathway in rat.

Baicalin is one of the active ingredients in the skullcap, with a variety of pharmacological effects, such as blood pressure reduction, sedation, liver-protection, gallbladder-protection, anti-bacteria, anti-inflammation, etc. The aim of this study was to investigate the potential cardioprotective effects of baicalin ameliorates isoproterenol-induced acute myocardial infarction (AMI) through inducible nitric oxide synthase (iNOS), inflammation, oxidative stress and P38MAPK passageway in rat. Rat model of AMI was induced by isoproterenol (100 mg/kg) and then treated baicalin (various does of baicalin: 1 mg/kg, 10 mg/kg and 100 mg/kg, respectively) for 24 h. Infarct size, the heart weight to body weight ratio and creatine kinase (CK), the MB isoenzyme of creatine kinase (CK-MB), lactate dehydrogenase (LDH) and cardiac troponin T (cTnT) of rats with AMI induced by isoproterenol were used to evaluate curative effect of baicalin on AMI. Meanwhile, iNOS and phosphorylation-p38 MAPK (p-p38) protein expressions, inflammatory factor and oxidative stress were inspected using western blot and commercial kits, respectively. In the present study, pre-treatment with baicalin (10 or 100 mg/kg) significantly ameliorated infarct size, the heart weight to body weight ratio and CK, CK-MB, LDH and cTnT levels in rats with AMI induced by isoproterenol. iNOS protein expression, the serum TNF-α, IL-6, MDA and SOD levels and p-38 protein expressions were significantly suppressed by treatment with baicalin (10 or 100 mg/kg). These results suggest that acute treatment with baicalin ameliorates AMI, iNOS, inflammation, oxidative stress and P38MAPK pathway in rat with AMI induced by isoproterenol.