Products with Anti-diabetic bioactivity
| Cat.No. | Product Name |
|---|---|
| BCN2691 | L-Arginine |
| L-Arginine is the nitrogen donor for synthesis of nitric oxide, a potent vasodilator that is deficient during times of sickle cell crisis. L-Arginine exhibits anti-atherosclerotic effect, L-arginine and soy enriched diet are effective in prevention of osteoporosis associated with diabetes mellitus. Exogenous L-Arginine could enhance neonate lymphocyte proliferation through an interleukin-2-independent pathway. | |
| BCN3480 | Alizarin 2-methyl ether |
| 1. Alizarin 2-methyl ether enhances adipocyte differentiation by up to 131% . 2. Alizarin 2-methyl ether could be beneficial in the treatment of diabetes. | |
| BCN3572 | 3',5'-Diprenylgenistein |
| 1. 3',5'-Diprenylgenistein inhibits protein tyrosine phosphatase 1B (PTP1B) activities, it can reduce muscle cell viability. 2. 3',5'-Diprenylgenistein exhibits significant glucose-uptake activity in basal and insulin-stimulated L6 myotubes. | |
| BCN3646 | Dehydroeburicoic acid |
| 1. Dehydroeburicoic acid treatment resulted in a marked decrease of tumor weight and size without any significant decrease in mice body weights. 2. Dehydroeburicoic acid induces necrotic cell death that involves Ca(2+) overload, mitochondrial dysfunction, and calpain activation in human glioblastomas. 3. Dehydroeburicoic acid and Eburicoic acid have antioxidant and anti-inflammatory activities by the decrease of inflammatory cytokines and an increase of antioxidant enzyme activity, can protect the liver from CCl4-induced hepatic damage. | |
| BCN3669 | Tilianin |
| 1. Tilianin has anti-inflammatory activity. 2. Tilianin has antiatherogenic activity. 3. Tilianin inhibits the tumor necrotic factor-K (TNF-K)-induced expression of VCAM-1 by 74% and reduces TNF-K-induced activation of nuclear factor-UB in cultured human umbilical vein endothelial cells (HUVECs). 4. Tilianin has antihypertensive and vasorelaxant activities, mediates relaxation and antihypertension mainly by an endothelium-dependent manner, probably due to NO release, and also through an endothelium-independent pathway by opening K+ channels. | |
