| Description |
Kazinol B, a prenylated flavan with a dimethyl pyrane ring, is an inhibitor of nitric oxide (NO) production. Kazinol B improves insulin sensitivity by enhancing glucose uptake via the insulin-Akt signaling pathway and AMPK activation. Kazinol B has the potential for diabetes mellitus research[1][2].
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| Related Catalog |
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| Target |
Akt
AMPK
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| In Vitro |
Kazinol B (2, 10 and 20 μM; 72 hours) shows no toxicity to adipocytes in 3T3-L1 cells[1]. Kazinol B (2-20 μM; 72 hours) dose-dependently increases lipid accumulation by 2.4-fold (at 20 μM) treatment as compared with MDI-treated cells[1]. Kazinol B (2-20 μM; 5 days) dose-dependently increases PPARγ and C/EBPα protein and mRNA levels in MDI-treated 3T3-L1 adipocytes. Kazinol B increases the mRNA level of adiponectin in a dose-dependent manner[1]. Kazinol B (2-20 μM; 24 hours) increases the retained 2ʹNBDG-fluorescence in cells in a dose-dependent manner in differentiated 3T3-L1 adipocytes and C2C12 myoblasts. Kazinol B dependently increases the MDI-stimulated GLUT4 mRNA level up to 4.7-fold as compared with MDI-only treated cells[1]. Kazinol B (10-20 μM; pre-treated for 1 h followed by 1 h insulin) dose-dependently increases insulin-dependent Akt phosphorylation. Kazinol B alone strongly induces Akt phosphorylation compared with untreated cells. Kazinol B also increased insulin-stimulated AMPK phosphorylation[1]. Kazinol B (6.25, 12.5, 25, 50 μM; 18 hours) dose-dependently reduces amounts of iNOS protein in macrophages (RAW 264.7 cells) activated by LPS (1 ug/mL)[2].
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| References |
[1]. Hyejin Lee, et al. Kazinol B from Broussonetia kazinoki improves insulin sensitivity via Akt and AMPK activation in 3T3-L1 adipocytes. Fitoterapia. 2016 Jul;112:90-6. [2]. Jae-Ha Ryu, et al. Fitoterapia. 2003 Jun;74(4):350-4.Inhibition of nitric oxide production on LPS-activated macrophages by kazinol B from Broussonetia kazinoki.
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