White crystalline powder
herbs of Justicia orbiculata
5-[(1S,3aR,4R,6aR)-4-(1,3-Benzodioxol-5-yloxy)tetrahydro-1H,3H-furo[3,4-c]fur-1-yl]-1,3-benzodioxol/5-[(1S,3aR,4R,6aR)-4-(2H-1,3-benzodioxol-5-yloxy)tetrahydro-1H,3H-furo[3,4-c]furan-1-yl]-2H-1,3-benzodioxole/Sesamolin/5-[(1S,3aR,4R,6aR)-4-(1,3-Benzodioxol-5-yloxy)tetrahydro-1H,3H-furo[3,4-c]furan-1-yl]-1,3-benzodioxole/(1S,3aR,4R,6aR)-5-[4-(1,3-benzodioxol-5-yloxy)tetrahydro-1H,3H-furo[3,4-c]furan-1-yl]-1,3-benzodioxole/5-[4-(1,3-Benzodioxolol-5-yloxy)tetrahydro-1H,3H-furo[3,4-c]furan-1-yl]-1,3-benzodioxole/1,3-Benzodioxole, 5-[(1S,3aR,4R,6aR)-4-(1,3-benzodioxol-5-yloxy)tetrahydro-1H,3H-furo[3,4-c]furan-1-yl]-/1,3-benzodioxol-5-yl (1R,3aR,4S,6aR)-4-(1,3-benzodioxol-5-yl)perhydrofuro[3,4-c]furan-1-yl ether
Methanol; Chloroform; Acetontrile; Ethyl Acetate; DMF
520.8±50.0 °C at 760 mmHg
93 - 94ºC (Decomposes)
HS Code Reference
Personal Projective Equipment
For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:526-07-8) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
In our previous study, we demonstrated that sesamolin can increase the level of cancer cell susceptibility to natural killer (NK) cell mediated cytolysis when it treats cancer cells. The present study attempted to demonstrate the direct influence of sesamolin on NK cells. To achieve the study goal, an NK cell (NK-92MI) or Raji cell was treated with sesamolin for use in the analysis of the cytolytic activity of NK cells. When NK-92MI cells were treated with sesamolin, the cytolysis activities of NK cells increased depending on the concentration of sesamolin. However, the highest cytolytic activity of NK cells was observed when Raji and NK-92MI cells were treated with sesamolin at 20 μg/mL and 40 μg/mL, respectively. Sesamolin also increased the expression of the degranulation marker, CD107a, on the surface of NK cells and the production of immune-activation cytokine, IFN-γ, from NK cells. The effects of sesamolin on NK cells were reproduced in the naïve NK cells. We found that sesamolin effects are triggered by the result of phosphorylation of the p38, ERK1/2 and JNK pathways in NK cells. Taken together, this study proved that NK cell activity can be increased by the stimulation of sesamolin on NK cells as well as cancer cells.
Copyright © 2018 Elsevier B.V. All rights reserved.
CD107a; IFN-γ; Natural killer cell; Raji; Sesamolin
Sesamolin affects both natural killer cells and cancer cells in order to create an optimal environment for cancer cell sensitization.
Lee SE1, Lee JK2.
Colorectal cancer (CRC) is a common malignant tumor that seriously threatens human health and quality of life. At present, the search for safe and more effective treatment for CRC has become necessary. The present study investigated the anti-proliferative and apoptotic effects of sesamolin on human colorectal cancer (HCT116) cells, and the underlying mechanism. Cell proliferation was determined using MTT assay, while the expressions of JAK2, STAT3 and p-STA3 were determined using Western blotting. The levels of expression of matrix metalloproteinases-1, 2 and 9 (MMP1, MMP2 and MMP9) were determined using real-time quantitative polymerase chain reaction (qRT-PCR). The degree of migration and invasion of the cells was assessed using wound healing assay. The results of MTT assay showed that sesamolin significantly and time- and dose-dependently inhibited the proliferation of HCT116 cells (p < 0.05). Treatment of HCT116 cells with sesamolin significantly inhibited their migratory ability (p < 0.05). The expressions of p-JAK2 and p-STAT3 were significantly down-regulated 48 h after 20 µM of JAK2 specific inhibitor (AG490) was added to HCT116 cells (p < 0.05). The expression of p-STAT3 was also significantly and dose-dependently down-regulated 6 h after treatment of HCT116 cells with sesamolin (p < 0.05). Sesamolin and AG490 had synergistic effect and their combination significantly down-regulated the expression of p-STAT3, when compared with sesamolin alone (p < 0.05). Treatment of HCT116 cells with sesamolin significantly and dose-dependently reduced the levels of IL-6-induced expressions of MMP-1, MMP-2 and MMP-9 (p < 0.05). These results suggest that sesamolin induces apoptosis in HCT116 cells and prevents cell invasion via inhibition of the JAK2/STAT3 signaling pathway.
Sesamolin exerts anti-proliferative and apoptotic effect on human colorectal cancer cells via inhibition of JAK2/STAT3 signaling pathway.
Wu D1, Wang XP2, Zhang W2.
2019 Jul 31
Melanin protects the skin against the harmful effects of ultraviolet irradiation. However, melanin overproduction can result in several aesthetic problems, including melasma, freckles, age spots and chloasma. Therefore, development of anti-melanogenic agents is important for the prevention of serious hyperpigmentation diseases. Sesamolin is a lignan compound isolated from sesame seeds with several beneficial properties, including potential for melanin inhibition.
The aim of this study was to evaluate the anti-melanogenic effect of sesamolin in cell culture in vitro and the underlying mechanism of inhibition using molecular docking simulation.
Melanogenesis was induced by 3-isobutyl-1-methylxanthine in B16F10 melanoma cells, and the inhibitory effects of sesamolin were evaluated using zymography, a tyrosinase inhibitory activity assay, western blotting, and real-time reverse transcription-polymerase chain reaction analysis. Docking simulations between sesamolin and tyrosinase were performed using Autodock vina.
Sesamolin significantly inhibited the expression of melanogenesis-related factors tyrosinase, and tyrosinase-related proteins 1 and 2 at the mRNA and protein levels. Treatment of melanoma cells with 50 µM sesamolin demonstrated the strongest inhibition against intercellular tyrosinase and melanin synthesis without exerting cytotoxic effects. Sesamolin significantly reduced mushroom tyrosinase activity in a dose-dependent manner via a competitive inhibition mechanism. Tyrosinase docking simulations supported that sesamolin (-6.5 kcal/mol) bound to the active site of tyrosinase more strongly than the positive control (arbutin, -5.7 kcal/mol).
Sesamolin could be developed as a melanogenesis inhibiting agent owing to its dual function in blocking the generation of melanogenesis-related enzymes and inhibiting the enzymatic response of tyrosinase.
Copyright© Bentham Science Publishers; For any queries, please email at email@example.com.
Sesamolin; anti-melanogenesis; docking simulation; melanogenesis; melanogenesis-related protein; tyrosinase.
Inhibitory Effect of Sesamolin on Melanogenesis in B16F10 Cells Determined by In Vitro and Molecular Docking Analyses.
Baek SH1,2, Kang MG2, Park D1,2.