The fixed structure of Licochalcone A by α, β-unsaturated ketone is necessary for anti-inflammatory activity through the inhibition of NF-κB activation

Funakoshi‐Tago, Megumi; Nakamura, Kei; Tsuruya, Rina; Hatanaka, Masashi; Mashino, Tadahiko; Sonoda, Yoshiko; Kimura, Tadashi

doi:10.1016/j.intimp.2010.02.003

Cited by 42 publications

(26 citation statements)

References 30 publications

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“…In fact, we could observe covalent binding between licochalcone A and cysteine, and it has been shown that Cys179 in IKKβ is an important amino acid residue for inhibition of IKKβ-mediated nuclear factor-κB activation by licochalcone A [20]. Furthermore, a reduced licochalcone A that lacks a double bond failed to inhibit IKK-mediated nuclear factor-κB activation [30]. These reports suggest the possibility that licochalcone A binds to the cysteine residues of various proteins by the Michael addition reaction.…”

Section: Discussionmentioning

confidence: 99%

Licochalcones extracted from Glycyrrhiza inflata inhibit platelet aggregation accompanied by inhibition of COX-1 activity

et al. 2017

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Licochalcones extracted from Glycyrrhiza inflata are known to have a variety of biological properties such as anti-inflammatory, anti-bacterial, and anti-tumor activities, but their action on platelet aggregation has not yet been reported. Therefore, in this study we investigated the effects of licochalcones on platelet aggregation. Collagen and U46619, a thromboxane A2 receptor agonist, caused rabbit platelet aggregation, which was reversed by pretreatment with licochalcones A, C and D in concentration-dependent manners. Among these compounds, licochalcone A caused the most potent inhibitory effect on collagen-induced platelet aggregation. However, the licochalcones showed marginal inhibitory effects on thrombin or ADP-induced platelet aggregation. In addition to rabbit platelets, licochalcone A attenuated collagen-induced aggregation in human platelets. Because licochalcone A also inhibited arachidonic acid-induced platelet aggregation and production of thromboxane A2 induced by collagen in intact platelets, we further examined the direct interaction of licochalcone A with cyclooxygenase (COX)-1. As expected, licochalcone A caused an inhibitory effect on both COX-1 and COX-2 in vitro. Regarding the effect of licochalcone A on COX-1 enzyme reaction kinetics, although licochalcone A showed a stronger inhibition of prostaglandin E2 synthesis induced by lower concentrations of arachidonic acid, Vmax values in the presence or absence of licochalcone A were comparable, suggesting that it competes with arachidonic acid at the same binding site on COX-1. These results suggest that licochalcones inhibit collagen-induced platelet aggregation accompanied by inhibition of COX-1 activity.

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Section: Discussionmentioning

confidence: 99%

Licochalcones extracted from Glycyrrhiza inflata inhibit platelet aggregation accompanied by inhibition of COX-1 activity

et al. 2017

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“…Then, at 3 h, 6 h, 12 h, 18 h, 24 h and 48 h after injection, the state of thickening of the murine plantar hind paw was measured using a micrometer (accuracy 0.01 mm) (Mitutoyo) as described previously [22]. Furthermore, 6-week-old male Jcl-ICR mice (30-32 g) were injected subcutaneously into the right and left plantar hind paws with Apigenin, Lutelin and Fisetin (25 mg/kg, 50 mg/kg) or control vehicle (DMSO).…”

Section: Carrageenan-induced Paw Inflammation In Micementioning

confidence: 99%

Anti-inflammatory activity of structurally related flavonoids, Apigenin, Luteolin and Fisetin

Funakoshi‐Tago

Nakamura

Tago

et al. 2011

International Immunopharmacology

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138

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“…Licorice is one of the most commonly prescribed herbs in Chinese Traditional Medicine, and has been used for >2,000 years. The effects of licorice have been reported on various diseases, ranging from microbial infection to cancer (5)(6)(7). However, since herbs usually contain numerous chemical compositions, the mechanism of action of these herbs is currently unclear.…”

Section: Introductionmentioning

confidence: 99%

Licochalcone A induces T24 bladder cancer cell apoptosis by increasing intracellular calcium levels

Yang

Jiang

Yang

et al. 2016

Molecular Medicine Reports

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Abstract. Licochalcone A (LCA) has been reported to significantly inhibit cell proliferation, increase reactive oxygen species (ROS) levels, and induce apoptosis of T24 human bladder cancer cells via mitochondria and endoplasmic reticulum (ER) stress-triggered signaling pathways. Based on these findings, the present study aimed to investigate the mechanisms by which LCA induces apoptosis of T24 cells. Cultured T24 cells were treated with LCA, and cell viability was measured using the sulforhodamine B assay. Apoptosis was detected by flow cytometry with Annexin V/propidium iodide staining, and by fluorescent microscopy with Hoechst 33258 staining. The levels of intracellular free calcium ions were determined using Fluo-3 AM dye marker. Intracellular ROS levels were assessed using the 2' ,7'-dichlorodihydrofluorescein diacetate probe assay. The mitochondrial membrane potential was measured using 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethyl benzimidazole carbocyanine iodide. Furthermore, the mRNA expression levels of B-cell lymphoma (Bcl)-extra large, Bcl-2-associated X protein, Bcl-2-interacting mediator of cell death, apoptotic protease activating factor-1 (Apaf-1), calpain 2, cysteinyl aspartate specific proteinase (caspase)-3, caspase-4 and caspase-9 were determined using reverse transcription semiquantitative and quantitative polymerase chain reaction analyses. Treatment with LCA inhibited proliferation and induced apoptosis of T24 cells, and increased intracellular Ca 2+ levels and ROS production. Furthermore, LCA induced mitochondrial dysfunction, decreased mitochondrial membrane potential, and increased the mRNA expression levels of Apaf-1, caspase-9 and caspase-3. Exposure of T24 cells to LCA also triggered calpain 2 and caspase-4 activation, resulting in apoptosis. These findings indicated that LCA increased intracellular Ca 2+ levels, which may be associated with mitochondrial dysfunction. In addition, the ER stress pathway may be considered an important mechanism by which LCA induces apoptosis of T24 bladder cancer cells. IntroductionNatural herbal medicines have long been used to treat cancer. Biomedical research and cancer treatment clinical trials have provided evidence regarding the use of herbal medicines; therefore, they are increasingly being accepted as a complementary and alternative treatment (1). In addition, natural medicines have been reported to have an important role in human health, particularly certain well-studied plants, including Taxus chinensis (Taxus madia) (2), Radix Sophorae flavescentis (Sophora flavescens) (3), Alkanna tinctoria, Lithospermum erythrorhizon and licorice (Glycyrrhiza L) (4). Licorice is one of the most commonly prescribed herbs in Chinese Traditional Medicine, and has been used for >2,000 years. The effects of licorice have been reported on various diseases, ranging from microbial infection to cancer (5-7). However, since herbs usually contain numerous chemical compositions, the mechanism of action of these herbs is currently unclear. Recently, several chemical ing...

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The fixed structure of Licochalcone A by α, β-unsaturated ketone is necessary for anti-inflammatory activity through the inhibition of NF-κB activation

Cited by 42 publications

References 30 publications

Licochalcones extracted from Glycyrrhiza inflata inhibit platelet aggregation accompanied by inhibition of COX-1 activity

Licochalcones extracted from Glycyrrhiza inflata inhibit platelet aggregation accompanied by inhibition of COX-1 activity

Anti-inflammatory activity of structurally related flavonoids, Apigenin, Luteolin and Fisetin

Licochalcone A induces T24 bladder cancer cell apoptosis by increasing intracellular calcium levels

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