Advances in the pharmacological activities and mechanisms of diosgenin / 中国天然药物

Diosgenin, a well-known steroid sapogenin derived from plants, has been used as a starting material for production of steroidal hormones. The present review will summarize published literature concerning pharmacological potential of diosgenin, and the underlying mechanisms of actions. Diosgenin has shown a vast range of pharmacological activities in preclinical studies. It exhibits anticancer, cardiovascular protective, anti-diabetes, neuroprotective, immunomodulatory, estrogenic, and skin protective effects, mainly by inducing apoptosis, suppressing malignant transformation, decreasing oxidative stress, preventing inflammatory events, promoting cellular differentiation/proliferation, and regulating T-cell immune response, etc. It interferes with cell death pathways and their regulators to induce apoptosis. Diosgenin antagonizes tumor metastasis by modulating epithelial-mesenchymal transition and actin cytoskeleton to change cellular motility, suppressing degradation of matrix barrier, and inhibiting angiogenesis. Additionally, diosgenin improves antioxidant status and inhibits lipid peroxidation. Its anti-inflammatory activity is through inhibiting production of pro-inflammatory cytokines, enzymes and adhesion molecules. Furthermore, diosgenin drives cellular growth/differentiation through the estrogen receptor (ER) cascade and transcriptional factor PPARγ. In summary, these mechanistic studies provide a basis for further development of this compound for pharmacotherapy of various diseases.

Change and significance of nuclear factor-kappaB in adriamycin induced cardiomyopathy in rats.

BACKGROUND: This study aimed at investigating the change and significance of nuclear factor-kappaB (NF-kappaB) in cardiomyopathy induced by adriamycin (ADR) in rats. METHODS: Sixty male Wistar rats were randomly divided into three groups: control, ADR and ADR + pyrrolidine dithiocarbamate (PDTC) groups. After 30-day experiment, myocardial histopathological observation was performed. Location and distribution of NF-kappaB p50 was examined by immunohistochemical assay. Expression of NF-kappaB p50 protein was examined by immunobolt assay. Electrophoretic Mobility Shift Assay examined activity of NF-kappaB; Myocardium p53 gene expression was examined by RT-PCR analysis. RESULTS: The myocardial lesions of rats were less pronounced in ADR + PDTC group than in ADR group. Compared with control group, there were many myocardium nucleuses, which expressed NF-kappaB p50 and distribute under epicardium. Expression of NF-kappaB p50 protein in nucleus increased significantly in ADR group. The NF-kappaB binding activity increased significantly in ADR group. Myocardium expressions of p53 mRNA increased in ADR group. CONCLUSIONS: The NF-kappaB binding activity increased significantly in cardiomyopathy induced by ADR in rats. Moreover, NF-kappaB plays an important role in causing degeneration of myocardial tissue and regulating expression of related-apoptosis genes.