Antidiabetic effects of selenium-enriched Bifidobacterium longum DD98 in type 2 diabetes model of mice.

Both selenium and probiotics have shown antidiabetic effects in a type 2 diabetes model. The objective of this study is to investigate the alleviating effects of selenium-enriched Bifidobacterium longum DD98 (Se-B. longum DD98) on diabetes in mice and explore the possible underlying mechanism. A type 2 diabetes model was established using a high-fat diet and streptozotocin (STZ) injection in mice. To investigate the beneficial effects of Se-B. longum DD98, diabetic mice were then treated with B. longum DD98, Se-B. longum DD98, or sodium selenite (Na2SeO3) for three weeks. The results suggested that all three treatments could reduce the levels of fasting blood glucose (FBG), glycated hemoglobin (HbA1c), insulin and leptin, improve glucose tolerance, regulate lipid metabolism, and protect against the impairment of the liver and pancreas, while Se-B. longum DD98 showed a greater effect on relieving the above mentioned symptoms of type 2 diabetes in mice. Furthermore, this effect was associated with butyrate production and inflammatory response. Se-B. longum DD98 better increased the level of butyrate in feces and decreased the levels of proinflammatory cytokines in the pancreas compared with B. longum DD98 and Na2SeO3, leading to ameliorative insulin resistance. Se-B. longum DD98 also improved the glucagon like peptide-1 (GLP-1) level in serum and intestinal cells, which protected the pancreatic ß-islet cells from damage induced by type 2 diabetes. These results demonstrated that Na2SeO3, B. longum DD98, or Se-B. longum DD98 could alleviate the progression of type 2 diabetes in mice. Se-B. longum DD98 showed greater antidiabetic effects than the other two treatments, and could be considered as a promising candidate for treating type 2 diabetes.

Total flavonoid aglycones extract in Radix scutellariae inhibits lung carcinoma and lung metastasis by affecting cell cycle and DNA synthesis.

ETHNOPHARMACOLOGICAL RELEVANCE: Radix Scutellariae (Scutellaria baicalensis Georgi, RS), a traditional herbal medicine commonly used to treat inflammation, hypertension, cardiovascular disease, bacterial and viral infections, is reported to treat lung cancer by supplements of modern medicine. The total flavonoid aglycones extract (TFAE) from RS is the most important composition for the pharmacodynamic effects. The present study was designed to evaluate the anti-lung tumor effect of TFAE on A549 cells and A549 cell nude mice xenografts. The aim of the study is to investigate the effect and mechanism of TFAE treating non-small cell lung cancer both in vitro and in vivo. MATERIALS AND METHODS: The anti-tumor activity of TFAE in vitro was investigated using the MTT assay. The changes of cell invasion and migration were detected by Transwell assay and tube formation experiments were used to detect the anti-angiogenic effect. The anti-tumor effects of TFAE in vivo were evaluated in A549 cell nude mice xenografts. The mechanism of TFAE was detected by flow cytometry technology, western blot assay and immuno-histochemistry assay. RESULTS: In vitro, TFAE inhibited the proliferation, invasion and migration of A549 cells in a dose- and time-dependent manner. In vivo, TFAE by oral administration at 100mg/kg for 30 days decreased the tumor volume and tumor weight in A549 cell xenograft by 25.5% with no statistical significance (P<0.05) compared to the cis-platinum positive control group (30.0%). The cell cycle and DNA synthesis experiment illustrated that TFAE could induce A549 cell cycle to arreste in S phase and DNA synthesis in A549 cells be inhibited, while TFAE had no influence on apoptosis of A549 cells. Western Blot assay demonstrated that the treatment of TFAE could make Cyclin D1 decrease and p53 increase both in vitro and in vivo. CONCLUSION: TFAE displayed the inhibition effects of non-small cell lung cancer both in vitro and in vivo and the underlying mechanism might be related to the increased p53 protein expression and decreased Cyclin D1 expression, leading to cell cycle arrested in S phase and the decrease of DNA synthesis.