ABSTRACT
PURPOSE: Although numerous clinical neuroimaging studies have demonstrated that there are functional abnormalities of motor-related regions in patients with Parkinson's disease (PD) by resting-state functional magnetic resonance imaging (fMRI), little studies have explored the causal interactions within these motor-related regions. The present study aimed to examine Granger causality connectivity patterns within motor-related regions in PD patients. METHODS: Resting-state fMRI was conducted to investigate the causal connectivity differences within motor-related regions between 17 PD patients and 17 matched healthy controls. Subsequently, the relationship between the Unified Parkinson's Disease Rating Scale scores and causal connectivity values within motor-related regions was examined in PD patients. RESULTS: An increased causal connectivity from the left premotor cortex (PMC) to right primary motor cortex (M1) was found in PD patients compared with that of healthy controls. Also, increased causal flow from the PMC to M1 was negatively correlated with motor scores. CONCLUSION: PD patients have abnormal causal connectivity in specific motor-related regions, which may reflect a compensatory role of motor deficits in PD patients.
Subject(s)
Motor Cortex/diagnostic imaging , Motor Cortex/physiopathology , Parkinson Disease/diagnostic imaging , Parkinson Disease/physiopathology , Brain Mapping , Case-Control Studies , Female , Humans , Magnetic Resonance Imaging , Male , Middle Aged , Motor Activity/physiology , Neural Pathways/diagnostic imaging , Neural Pathways/physiopathology , Rest/physiologyABSTRACT
A water-soluble polysaccharide, named as JRP1, was extracted and fractioned from the epicarp of immature fruit of Juglans mandshurica Maxim. The determination of the monosaccharide composition in JRP1 with gas chromatography (GC) showed that JRP1 was composed of Gal (43.1%), Glu (23.6%), Ara (16.2%), Rha (9.8%) and Fru (7.3%). The results in vitro showed that 25, 50 and 100 µg/mL of JRP1 could present a significant inhibition on the growth of S180 cells, and furthermore, a significant improvement on the proliferation ability of lymphocytes and the phagocytic activity of macrophages. The results in vivo showed that compared with those in the control group, the inhibition rates of different doses of JRP1 on S180 cells in the tumor-bearing mice were 35.3%, 40.6% and 48.1%, respectively, and serum immune cytokine levels such as IL-2, TNF-α and IFN-γ were significantly improved. Our results confirm that JRP1 has the activities of effective antitumor and immunomodulatory function.
Subject(s)
Antineoplastic Agents, Phytogenic/pharmacology , Immunologic Factors/pharmacology , Juglans/chemistry , Plant Extracts/pharmacology , Polysaccharides/pharmacology , Animals , Antineoplastic Agents, Phytogenic/chemistry , Cell Line, Tumor , Disease Models, Animal , Female , Immunologic Factors/chemistry , Lymphocytes/drug effects , Lymphocytes/immunology , Macrophages/drug effects , Macrophages/immunology , Male , Mice , Neoplasms/drug therapy , Neoplasms/immunology , Neoplasms/pathology , Organ Size/drug effects , Phagocytosis/drug effects , Phagocytosis/immunology , Plant Extracts/chemistry , Polysaccharides/chemistry , Tumor Burden/drug effectsABSTRACT
Glioblastoma multiforme (GBM) is one of the most common glial cell tumors and has drawn more and more attention in the clinic in recent years. Brucine has been reported to significantly suppress gastric cancer, lung cancer, and prostate cancer growth in vivo by inducing cell apoptosis. Here, the effects of brucine on U251 human glioma cell growth were investigated in vitro by cell proliferation assay, FACs, and qPCR in a xenograft tumor model. Treatment with brucine reduced the expression of BCL-2 and cyclooxygenase-2 (COX-2), while upregulated BAX expression in U251 human glioma cells resulted in reduced glioma cell survival rate and inhibited the growth of xenograft tumors. We concluded that brucine has a suppressive effect on U251 human glioma cells in vitro and in vivo, which could help in understanding the role of brucine in glioma cells and guiding drug use in the clinic.