Background/Aims: Raddeanin A (RA), an active pharmacological ingredient from Anemone raddeana Regel, plays an important role in tumor suppression. In this study, we assessed the potentially therapeutic effect of RA on glioblastoma and its underlying mechanisms. Methods: Cell viability was examined using the MTT assay. Invasive and migratory capacities were examined using Transwell and wound healing assays. Apoptosis was determined by Hoechst staining, flow cytometry, DCFH-fluorescent probe and immunohistochemical staining. Autophagy was detected by transmission electron microscopy and western blotting. A U251 glioma xenograft model was established to evaluate the effect of RA in vivo. Results: The data demonstrated that RA inhibited viability, and abrogated the invasive/migratory abilities of glioblastoma cells. In addition, RA induced apoptosis by reactive oxygen species (ROS)/ Jun N-terminal kinase (JNK) signaling in glioblastoma. Conversely, the antioxidant N-Acetyl-L-cysteine (NAC) and pan-caspase inhibitor z-VAD-fmk attenuated RA-induced apoptosis by scavenging ROS and inactivating caspase-3. Furthermore, the inhibition of autophagy by 3-MA exacerbated apoptosis through ROS generation and JNK phosphorylation. In vivo, RA exhibited a curative effect on U251-derived xenografts in nude mice. Conclusions: The results of this study suggest that RA suppressed the growth of glioblastoma, thus serving as a promising and potential strategy for glioblastoma chemotherapy.

ABSTRACT. We aimed at observing the effects of high thoracic epidural anesthesia (HTEA) on cardiac structure and function, heart rate variability (HRV), and QT interval variation (QTV) in ischemic cardiomyopathy (ICM) patients with chronic heart failure. We divided 30 ICM patients into HTEA (N = 16) and control (N = 14) groups.The control group was treated with medication, and the HTEA group was treated with HTEA and medication for 4 weeks. We measured the changes in the left-ventricular end-diastolic diameter (LVEDd) and left-ventricular ejection fraction (LVEF) before and after treatment by using echocardiography and examined changes in HRV and QTV using ambulatory electrocardiogram. HTEA significantly narrowed the LVEDd, improved LVEF, significantly increased the HRV, and significantly reduced the QTV in the ICM group compared to the control group. HTEA significantly narrowed the ventricular chamber diameter size of ICM patients, enhanced myocardial contractility, increased myocardial electrical stability, and improved the cardiac structure and function.

Fluoroacetic acid (FAcOH) was once a highly toxic rodenticide widely used in the world. In the past, studies on the toxicity of FAcOH have focused on animal experiments. The toxicity of FAcOH to humans and the changes of FAcOH in plasma have not been studied. Therefore, the present study aimed to describe the changes of plasma FAcOH concentrations, hematological, and biochemical characteristics in patients with FAcOH intoxication. According to clinical symptoms, 68 patients from the emergency department were divided into different groups: convulsion group, unconsciousness group, death group, and control groups. Plasma FAcOH concentrations, hematological, and biochemical parameters were investigated. Results demonstrated that patients in the convulsion group and the unconsciousness group had a significant increase ( p < 0.01) in the level of neuron-specific enolase (NSE), creatine kinase MB (CKMB), glucose (GLU), and white blood cell count (WBC) and a significant decrease ( p < 0.01) in serum potassium compared with the control group, respectively. Moreover, patients in the death group had a significant increase ( p < 0.01) in the level of NSE, CKMB, N-terminal pro-brain natriuretic peptide, GLU, and WBC and a significant decrease ( p < 0.01) in serum potassium and total calcium compared with the survival group. The concentrations of FAcOH in plasma in the convulsion group, the unconsciousness group, and the death group were 72.31 ± 42.29, 118.33 ± 55.41, and 163.78 ± 43.32 μg/mL, respectively. These changes and the plasma FAcOH concentrations may increase our understanding of the toxicity of FAcOH to humans and may help doctors to judge the clinical prognosis of patients with FAcOH intoxication.