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Licochalcone E Sale

(Synonyms: 甘草查尔酮E) 目录号 : GC36447

Licochalcone E 是可从Glycyrrhiza inflate 中提取到的黄酮类化合物,通过抑制AKT 和 MAPK 的激活来抑制NF-κB 和 AP-1 的转录活性。

Licochalcone E Chemical Structure

Cas No.:864232-34-8

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产品描述

Licochalcone E, a flavonoid compound isolated from Glycyrrhiza inflate, inhibits NF-κB and AP-1 transcriptional activity through the inhibition of AKT and MAPK activation[1]. AKT, MAPK, NF-κB[1].

[1]. Lee HN, et al. Mechanisms by which licochalcone e exhibits potent anti-inflammatory properties: studies with phorbol ester-treated mouse skin and lipopolysaccharide-stimulated murine macrophages. Int J Mol Sci. 2013 May 24;14(6):10926-43.

Chemical Properties

Cas No. 864232-34-8 SDF
别名 甘草查尔酮E
Canonical SMILES O=C(C1=CC=C(O)C=C1)/C=C/C2=CC([C@@H](C)C(C)=C)=C(O)C=C2OC
分子式 C21H22O4 分子量 338.4
溶解度 DMSO: 125 mg/mL (369.39 mM) 储存条件 4°C, protect from light
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5 mM 0.591 mL 2.9551 mL 5.9102 mL
10 mM 0.2955 mL 1.4775 mL 2.9551 mL
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Research Update

Licochalcone E improves insulin sensitivity in palmitic acid-treated HepG2 cells through inhibition of the NLRP3 signaling pathway

Int Immunopharmacol 2021 Oct;99:107923.PMID:34229177DOI:10.1016/j.intimp.2021.107923.

Our previous research demonstrated that compound Licochalcone E can reduce glucose tolerance and lipid metabolism in diabetic rats, although its mechanism remains unknown. Here, we used palmitic acid (PA) to establish a PA-treated HepG2 model, and then examined glucose uptake, glucose consumption, and blood lipids to evaluate the effects of Licochalcone E within the safe dose range in the model. Polymerase chain reaction (PCR) was used to detect the expression levels of key genes associated with liver gluconeogenesis; enzyme-linked immunosorbent assay (ELISA) was deployed to evaluate the concentration of inflammatory factors; and laser confocal microscopy and western blot were used to determine the levels of reactive oxygen species (ROS) and NLRP3 inflammasome signaling pathway-related proteins, respectively. Finally, molecular simulations were exploited to validate the interaction between Licochalcone E and the NLRP3 inflammasome. The results demonstrated that Licochalcone E showed no toxicity in the dose range of 2.5-40 μM. In this dose range, Licochalcone E substantially increased the uptake and consumption of glucose in the insulin resistance model and dose-dependently reduced the concentration of total cholesterol. The PCR results indicated that Licochalcone E dose-dependently reduced the expression of Glucose-6-phosphatase (G6Pase) and Phosphoenolpyruvate carboxykinase (PEPCK) genes and increased the expression of Glucose Transporter 4 (Glut4) in PA-treated HepG2. Moreover, the ELISA results revealed that Licochalcone E significantly reduced the expression of TNF-α, IL-1β, and IL-18. Confocal microscopy results showed that Licochalcone E dramatically reduced the generation of ROS and the expressions of NLRP3 and its downstream caspase-1 in PA-treated HepG2 model. Western blot results further indicated that Licochalcone E significantly reduced the expression of NLRP3, caspase-1 and IL-1β in the model. Additionally, molecular simulations demonstrated that Licochalcone E has good binding affinity for the NLPR3 inflammasome. We concluded that Licochalcone E has the potential to be used as an insulin sensitizer by reducing the release of ROS and inflammatory factors following inhibition of the NLPR3 signaling pathway.

Licochalcone E inhibits trxR1 expression, alters Nrf2/STAT6 signal, and induces antitumor effects in vitro against human SH-SY5Y and SK-N-BE(2) neuroblastoma cells

Environ Toxicol 2022 May;37(5):1173-1184.PMID:35092341DOI:10.1002/tox.23474.

Neuroblastoma (NB) is the most common solid tumor of the sympathetic nervous system (SNS) arising in childhood less than 15 years age. Licochalcone (Lic) is known to show inhibitory effects in cancer growth, and there has evidence suggested that Lic A inhibits hypoxic induced NB SK-N-SH cell proliferation. However, it is unclear whether LicE exerts similar effects in NB and the associated molecular mechanism of Lic in neuroblastoma is still unclear. In the current study, we found that LicE at the concentration 2, 4 and 6 μM all induced a profound reduction in cell viability, colony formation and cell proliferation. Next, LicE treatment effectively promoted cell apoptosis, inhibited cell migration and invasion. LicE significantly suppressed trxR1 expression, activated Nrf2 expression and inhibited STAT6 expression in SH-SY5Y and SK-N-BE(2) NB cells. We further identified that trxR1, STAT6 overexpression or Nrf2 silence reversed the antitumor effects of LicE in human SH-SY5Y and SK-N-BE(2) NB cells. Finally, LicE treatment significantly inhibited tumor growth in nude mice carrying a SK-N-SH cell xenograft. These results provide new insights into the effects and highlighting a novel mechanism of LicE through regulating trxR1/Nrf2/STAT6 signal pathway in NB.

Licochalcone E has an antidiabetic effect

J Nutr Biochem 2012 Jul;23(7):759-67.PMID:21840191DOI:10.1016/j.jnutbio.2011.03.021.

Licochalcone E (lico E) is a retrochalcone isolated from the root of Glycyrrhiza inflata. Retrochalcone compounds evidence a variety of pharmacological profiles, including anticancer, antiparasitic, antibacterial, antioxidative and superoxide-scavenging properties. In this study, we evaluated the biological effects of lico E on adipocyte differentiation in vitro and obesity-related diabetes in vivo. We employed 3T3-L1 preadipocyte and C3H10T1/2 stem cells for in vitro adipocyte differentiation study and diet-induced diabetic mice for in vivo study. The presence of lico E during adipogenesis induced adipocyte differentiation to a significant degree, particularly at the early induction stage. Licochalcone E evidenced weak, but significant, peroxisome proliferator-activated receptor gamma (PPARγ) ligand-binding activity. Two weeks of lico E treatment lowered blood glucose levels and serum triglyceride levels in the diabetic mice. Additionally, treatment with lico E resulted in marked reductions in adipocyte size and increases in the mRNA expression levels of PPARγ in white adipose tissue (WAT). Licochalcone E was also shown to significantly stimulate Akt signaling in epididymal WAT. In conclusion, lico E increases the levels of PPARγ expression, at least in part, via the stimulation of Akt signals and functions as a PPARγ partial agonist, and this increased PPARγ expression enhances adipocyte differentiation and increases the population of small adipocytes, resulting in improvements in hyperglycemia and hyperlipidemia under diabetic conditions.

Licochalcone E, a β-Amyloid Aggregation Inhibitor, Regulates Microglial M1/M2 Polarization via Inhibition of CTL1-Mediated Choline Uptake

Biomolecules 2023 Jan 17;13(2):191.PMID:36830561DOI:10.3390/biom13020191.

Alzheimer's disease (AD) is thought to be a series of neuroinflammatory diseases caused by abnormal deposits of amyloid-β (Aβ) and tau protein in the brain as part of its etiology. We focused on Aβ aggregation and M1 and M2 microglial polarity in microglia to search for novel therapeutic agents. It has been reported that the inhibition of choline uptake via choline transporter-like protein 1 (CTL1) in microglia preferentially induces M2 microglial polarity. However, the role of the choline transport system on the regulation of microglial M1/M2 polarity in AD is not fully understood. Licochalcones (Licos) A-E, flavonoids extracted from licorice, have been reported to have immunological anti-inflammatory effects, and Lico A inhibits Aβ aggregation. In this study, we compared the efficacy of five Licos, from Lico A to E, at inhibiting Aβ1-42 aggregation. Among the five Licos, Lico E was selected to investigate the relationship between the inhibition of choline uptake and microglial M1/M2 polarization using the immortalized mouse microglial cell line SIM-A9. We newly found that Lico E inhibited choline uptake and Aβ1-42 aggregation in SIM-A9 cells in a concentration-dependent manner, suggesting that the inhibitory effect of Lico E on choline uptake is mediated by CTL1. The mRNA expression of tumor necrosis factor (TNF-α), a marker of M1 microglia, was increased by Aβ1-42, and its effect was inhibited by choline deprivation and Lico E in a concentration-dependent manner. In contrast, the mRNA expression of arginase-1 (Arg-1), a marker of M2 microglia, was increased by IL-4, and its effect was enhanced by choline deprivation and Lico E. We found that Lico E has an inhibitory effect on Aβ aggregation and promotes polarity from M1 to M2 microglia via inhibition of the CTL1 function in microglia. Thus, Lico E may become a leading compound for a novel treatment of AD.

Licochalcone E reduces chronic allergic contact dermatitis and inhibits IL-12p40 production through down-regulation of NF-kappa B

Int Immunopharmacol 2010 Sep;10(9):1119-26.PMID:20601178DOI:10.1016/j.intimp.2010.06.015.

Licochalcone, a constituent of licorice, has antitumor, antimicrobial, and anti-inflammatory effects. Recently, Licochalcone E was isolated from the roots of Glycyrrhiza inflata and its biological functions are not fully examined. In this study, we investigated its ability to modulate production of IL-12p40, a common subunit of IL-12 and IL-23. Licochalcone E dose-dependently inhibited IL-12p40 production from lipopolysaccharide-stimulated RAW264.7 macrophage cells. The repressive effect was mapped to a region in the IL-12 gene promoter containing a binding site for NF-kappaB. Furthermore, Licochalcone E decreased binding to the NF-kappaB site in RAW264.7 macrophage cells. Using a chronic allergic contact dermatitis model induced by repeated application of oxazolone, we showed that Licochalcone E inhibited the increased IL-12p40 expression and ear thickness induced by oxazolone. Taken together, Licochalcone E inhibits IL-12p40 production and has therapeutic potential to reduce skin inflammation.