Gynostemma pentaphyllum (GP) is a natural plant resources for diabetes therapy, however, there is little research on the mechanisms of GP. The present study was undertaken to characterize if G. pentaphyllum saponins (GPs) is the principal active compound of GP responsible for anti-diabetes, and to examine the relativity between blood glucose modulate and antioxidation. The GPs-treated streptozotocin diabetic rats had a more effective hypoglycemic status than those of diabetic control rats, which also ameliorate dyslipidemia. GPs has increased SOD and GSH-px activities, and the spleen and thymus indexes in diabetic rats. The insulin levels in the GPs-treated groups were significantly higher than diabetic control group. Our finding provides a new insight into the application of GPs for the treatment of oxidative stress related diseases.

Tobacco-derived carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is a major environmental risk factor for the pathogenesis of human esophageal squamous cell carcinoma (ESCC). However, the molecular mechanisms by which tobacco induces ESCC are not well understood. Na+/Ca2+ exchanger 1 (NCX1) is a plasma membrane transporter protein that plays an essential role in maintaining cytosolic Ca2+ ([Ca2+]cyt) homeostasis under physiological conditions and is implicated in tumorigenesis as well. In this study, we found that NCX1 expression was significantly higher in ESCC primary tissues compared to the noncancerous tissues and was overexpressed in tumor samples from the smoking patients. The expression of NCX1 proteins was also significantly higher in human ESCC cell lines compared to normal esophageal epithelial cell line. Moreover, NNK potentiated the [Ca2+]cyt signaling induced by removal of extracellular Na+, which was abolished by KB-R7943 or SN-6. NNK dose-dependently promoted proliferation and migration of human ESCC cells induced by NCX1 activation. Therefore, NCX1 expression correlates with the smoking status of ESCC patients, and NNK activates the Ca2+ entry mode of NCX1 in ESCC cells, leading to cell proliferation and migration. Our findings suggest NCX1 protein is a novel potential target for ESCC therapy.

These results demonstrated that the magnetic drug system had a great potential to cross the blood-brain barrier and provided a noninvasive and effective therapeutic strategy for PD.

proliferation, tube formation and paracrine of EPCs were reduced in patients with permanent AF.