In this study, the authors investigated the anti-melanogenic effects of 3,8-dihydroxyquinoline (jineol) isolated from Scolopendra subspinipes mutilans, the mechanisms responsible for its inhibition of melanogenesis in melan-a cells, and its antioxidant efficacy. Mushroom tyrosinase activities and melanin contents were determined in melan-a cells, and the protein and mRNA levels of MITF, tyrosinase, TYRP-1, and TYRP-2 were assessed. Jineol exhibited significant, concentration-dependent antioxidant effects as determined by DPPH, ABTS, CUPRAC, and FRAP assays. Jineol significantly inhibited mushroom tyrosinase activity by functioning as an uncompetitive inhibitor, and markedly inhibited melanin production and intracellular tyrosinase activity in melan-a cells. In addition, jineol abolished the expressions of tyrosinase, TYRP-1, TYRP-2, and MITF, thereby blocking melanin production and interfering with the phosphorylations of ERK1/2 and p38. Furthermore, specific inhibitors of ERK1/2 and p38 prevented melanogenesis inhibition by jineol, and the proteasome inhibitor (MG-132) prevented jineol-induced reductions in cellular tyrosinase levels. Taken together, jineol was found to stimulate MAP-kinase (ERK1/2 and p38) phosphorylation and the proteolytic degradation pathway, which led to the degradations of MITF and tyrosinase, and to suppress the productions of melanin.
Glucose absorption from the gut and glucose uptake into muscles are vital for the regulation of glucose homeostasis. In the current study, we determined if gossypol (GSP) reduces postprandial hyperglycemia or enhances glucose uptake; we also investigated the molecular mechanisms underlying those processes in vitro and in vivo. GSP strongly and concentration dependently inhibited α-glucosidase by functioning as a competitive inhibitor with IC50 value of 0.67 ± 0.44. GSP activated the insulin receptor substrate 1 (IRS-1)/protein kinase B (Akt) signaling pathways and enhanced glucose uptake through the translocation of glucose transporter 4 (GLUT4) into plasma membrane in C2C12 myotubes. Pretreatment with a specific inhibitor attenuated the in vitro effects of GSP. We used a streptozotocin-induced diabetic mouse model to assess the antidiabetic potential of GSP. Consistent with the in vitro study, a higher dose of GSP (2.5 mg/kg−1) dramatically decreased the postprandial blood glucose levels associated with the upregulated expressions of GLUT4 and the IRS-1/Akt-mediated signaling cascade in skeletal muscle. GSP treatment also significantly boosted antioxidant enzyme expression and mitigated gluconeogenesis in the liver. Collectively, these data imply that GSP has the potential in managing and preventing diabetes by ameliorating glucose uptake and improving glucose homeostasis.
Scope: The aim of this study is to investigate the antidiabetic effect of lariciresinol (LSR) in C2C12 myotubes and streptozotocin (STZ)-induced diabetic mice. Methods and results: To investigate antidiabetic potential of LSR, 𝜶-glucosidase inhibitory assay, molecular docking, glucose uptake assay, western blot assay on antidiabetic biomarkers are performed. STZ-induced diabetic model is used for in vivo study by calculating oral glucose tolerance test, histochemical examination, and glycogen assay. LSR inhibits 𝜶-glucosidase activity with an IC 50 value of 6.97 ± 0.37 µM and acts as a competitive inhibitor with an inhibitory constant (Ki) value of 0.046 µM. In C2C12 cells, LSR activates insulin signaling leading to glucose transporter 4 (GLUT4) translocation and augmented glucose uptake. Furthermore, in Streptozotocin (STZ)-treated diabetic mice, 3 weeks of oral LSR administration (10 mg kg −1 ) considerably decrease blood glucose levels, while increasing insulin levels in an oral glucose tolerance test, improve pancreatic islet size, increase GLUT4 expression, and significantly enhance insulin signaling in skeletal muscle. LSR treatment also activates glycogen synthase kinase 3𝜷 (GSK-3𝜷) resulting in improved glycogen content. Conclusion: The findings indicate a potential usefulness for oral LSR in the management and prevention of diabetes by enhancing glucose homeostasis.
In order to assess whether the fine powder of Jeju citrus can be used for better quality characteristics in food processing, we first prepared ultra-fine powder C20 (20 mesh of citrus), C40 (40 mesh of citrus), and C100 (100 mesh of citrus). The mean particle size of C20, C40, and C100 were 662.6±176.9, 344.6±126.8, and 91.7±54.9 μm, respectively. The antioxidant activity measured by the 2,2-Diphenyl-1-picrylhydrazyl (DPPH) and 2,2′ -Azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt (ABTS) radical scavenging assay and ferric Reducing Antioxidant Power (FRAP) assay was the highest in C100. Moreover, increasing mesh of citrus increased the L* and b* values of citrus, but not the a* value of citrus. Using a prototype developed from the powder, we performed sensory tests for taste, color, texture, flavor and overall preference. C100 showed the highest score compared to C20 and C40 in the sensory evaluation. Particularly, C100 had excellent flavor among all the powders. Our results collectively indicate that the Jeju citrus supplementation has better quality characteristics during food processing; this may aid in the development of food ingredients for functional food materials. Furthermore, a high mesh of citrus provides better quality in citrus-based food processing.
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