White crystalline Powder
Artemisia annua,Atractylodes macrocephala,Dictamnus dasycarpus,Cirsium japonicum,Euphorbia fischeriana
7-hydroxy-6-methoxychromen-2-one/7-Hydroxy-6-methoxycoumarin/Scopoletine/Esculetin-6-methyl ether/6-Methylesculetin/6-Methoxyumbelliferone/Escopoletin/6-methoxy-7-hydroxy-coumarin/2H-1-Benzopyran-2-one, 7-hydroxy-6-methoxy-/Chrysatropic acid/Scopoletin/Gelseminic Acid/7-hydroxy-6-methoxy-2H-benzopyran-2-one/7-hydroxy-6-methoxy-2H-1-benzopyran-2-one/Scopoletol/β-Methylesculetin/6-O-Methylesculetin/7-Hydroxy-6-methoxy-2H-chromen-2-one/b-Methylesculetin/Murrayetin/7-Hydroxy-5-methoxycoumarin
413.5±45.0 °C at 760 mmHg
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provides coniferyl ferulate(CAS#:92-61-5) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
The aim of this study was to investigate whether scopoletin could inhibit the activities of the carbohydrate digestive enzymes, α-glucosidase and α-amylase, and reduce postprandial hyperglycemia in streptozotocin (STZ)-induced diabetes in mice. Scopoletin showed a distinct inhibitory effect on α-glucosidase and α-amylase. The half maximal inhibitory concentration (IC50) of scopoletin was 85.12 and 37.36 μM for α-glucosidase and α-amylase, respectively, which were lower values than those for acarbose. The increase in postprandial blood glucose levels was significantly suppressed in the scopoletin group compared to the control group of STZ-induced diabetes in mice. Moreover, the area under the curve significantly decreased with the administration of scopoletin in STZ-induced diabetes in mice. These results showed that scopoletin might help to lower postprandial hyperglycemia through inhibition of carbohydrate digestive enzymes.
Copyright © 2018 Elsevier B.V. All rights reserved
Diabetic mice; Postprandial hyperglycemia; Scopoletin; α-amylase; α-glucosidase
Scopoletin inhibits α-glucosidase in vitro and alleviates postprandial hyperglycemia in mice with diabetes.
Jang JH1, Park JE1, Han JS2.
2018 Sep 5
Irradiation of keratinocytes by ultraviolet B induces cytokine production, which in turn activates fibroblasts to produce cytokines and increase matrix metallopeptidase (MMP)‑1 protein expression. The present study investigated the effect and potential mechanisms of scopoletin on the regulation of MMP‑1 expression in fibroblasts. Scopoletin was isolated from Artemisia capillaris crude extract. Treatment of fibroblasts with scopoletin resulted in a decrease in the protein expression of MMP‑1 following stimulation with human keratinocyte (HaCaT) conditioned medium. To further explore the mechanism underlying this effect, the expression levels of proteins in the mitogen‑activated protein kinase (MAPK) and nuclear factor‑κB (NF‑κB) signaling pathways were evaluated via western blot analysis. The mRNA expression levels of interleukin (IL)‑1α and tumor necrosis factor (TNF) α were evaluated via reverse transcription‑quantitative polymerase chain reaction. The effect of scopoletin on cell viability was assessed with the MTT assay. The results demonstrated that scopoletin treatment markedly decreased MMP‑1, IL‑1α and TNFα mRNA expression in fibroblasts stimulated with HaCaT conditioned medium (40 mJ/cm2), without any apparent cell cytotoxicity, and in a dose‑dependent manner. In addition, western blot analysis demonstrated that scopoletin reduced the phosphorylation of p38 MAPK in fibroblasts. In summary, the present study demonstrated that scopoletin inhibited MMP‑1 and proinflammatory cytokine expression by inhibiting p38 MAPK phosphorylation. These findings suggest that scopoletin may have potential as a therapeutic agent to prevent and treat photoaging of the skin.
Scopoletin downregulates MMP‑1 expression in human fibroblasts via inhibition of p38 phosphorylation.
Kim HL1, Woo SM1, Choi WR1, Kim HS1, Yi C2, Kim KH1, Cheng J2, Yang SH3, Suh JW1.
Scopoletin was recently shown to stimulate melanogenesis through cAMP-response element-binding protein (CREB) phosphorylation. In this study, we investigated the molecular events of melanogenesis-induced by scopoletin. After exposure to scopoletin, the protein levels of tyrosinase and tyrosianse related protein-1 (TRP-1) were significantly increased in B16F10 cells. The mRNA levels of tyrosinase and microphthalmia-associated transcription factor (MITF) were also enhanced by scopoletin. cAMP production and phosphorylation of p38 mitogen-activated protein kinase (MAPK) were increased by scopoletin treatment. Scopoletin-mediated increase of intracellular melanin and tyrosinase expression were significantly attenuated by protein kinase A (PKA) inhibitors (H-89 and KT5720), while a protein kinase C (PKC) inhibitor (Ro-32-0432) had no effect and a p38 MAPK inhibitor (SB203580) partially blocked the scopoletin-induced intracellular melanin and tyrosinase expression. Moreover, scopoletin synergistically with cell-permeable cAMP analog (dibutyryl cAMP) significantly induced tyrosinase activity and melanin content in B16F10 cells. The silencing of p38 MAPK by small interfering RNA (siRNA) decreased the scopoletin-induced tyrosinase expression in B16F10 cells. These results suggest that scopoletin could induce melanin synthesis through the cAMP/PKA pathway and partially p38 MAPK activation in B16F10 cells.
cAMP; microphthalmia-associated transcription factor; p38 mitogen-activated protein kinase; scopoletin; small interfering RNA; tyrosinase
Scopoletin Stimulates Melanogenesis via cAMP/PKA Pathway and Partially p38 Activation.
Kim DS1, Cha SB1, Park MC2, Park SA3, Kim HS4, Woo WH5, Mun YJ1.
2017 Dec 1
Scopoletin is an inhibitor of acetylcholinesterase (AChE).