Tricetin
(Synonyms: 三粒小麦黄酮) 目录号 : GC64862
Tricetin 是一种有效的竞争性 Keap1-Nrf2 蛋白相互作用 (PPI) 抑制剂。Tricetin 作用于帕金森病模型，通过激活 Nrf2/HO-1 信号通路和阻止线粒体依赖性细胞凋亡 (apoptosis) 通路来保护 6-OHDA 诱导的神经毒性。
Cas No.:520-31-0
Sample solution is provided at 25 µL, 10mM.
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- Purity: >98.00%
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Tricetin is a potent competitive inhibitor of the Keap1-Nrf2 Protein Protein Interaction (PPI). Tricetin protects against 6-OHDA-induced neurotoxicity in Parkinson's disease model by activating Nrf2/HO-1 signaling pathway and preventing mitochondria-dependent apoptosis pathway[1].
Tricetin is mainly found in natural plants such as Ginkgo biloba L., Carica papaya L. and Murraya exotica L. Tricetin activates the Nrf2/HO-1 pathway to protect cells from oxidative stress. Tricetin possessed the protective effect on dopamine neurons of C. elegans. Tricetin has cytostatic properties and anti-metastatic activity of various solid tumors[1].Pretreatment with Tricetin (20, 40, and 80 μM; for 4 hours) significantly improves 6-OHDA (200 μM)-induced SH-SY5Y cells viability and suppresses mitochondria-mediated apoptosis[1].Tricetin (80 μM; for 1, 2 and 4 h) markedly decreased the expressions of p-JNK and p-p38[1].
[1]. Ren J, et al. Tricetin protects against 6-OHDA-induced neurotoxicity in Parkinson's disease model by activating Nrf2/HO-1 signaling pathway and preventing mitochondria-dependent apoptosis pathway. Toxicol Appl Pharmacol. 2019;378:114617.
| Cas No. | 520-31-0 | SDF | Download SDF |
| 别名 | 三粒小麦黄酮 | ||
| 分子式 | C15H10O7 | 分子量 | 302.24 |
| 溶解度 | 储存条件 | Store at -20°C | |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.3086 mL | 16.5431 mL | 33.0863 mL |
| 5 mM | 0.6617 mL | 3.3086 mL | 6.6173 mL |
| 10 mM | 0.3309 mL | 1.6543 mL | 3.3086 mL |
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动物平均体重 | g | |
每只动物给药体积 | ul | |
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| % DMSO % % Tween 80 % saline | ||||||||||
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2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
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Tricetin Suppresses Migration and Presenilin-1 Expression of Nasopharyngeal Carcinoma through Akt/GSK-3β Pathway
Am J Chin Med 2020;48(5):1203-1220.PMID:32668971DOI:10.1142/S0192415X20500597.
Lymph node migration results in poor prognoses for nasopharyngeal carcinoma (NPC) patients. Tricetin, a flavonoid derivative, regulates tumorigenesis activity through its antiproliferative and antimetastatic properties. However, the molecular mechanism of Tricetin affecting the migration and invasion of NPC cells remains poorly understood. In this paper, we examined the antimetastatic properties of Tricetin in human NPC cells. Our results demonstrated that Tricetin at noncytotoxic concentrations (0-80 3M) noticeably reduced the migration and invasion of NPC cells (HONE-1, NPC-39, and NPC-BM). Moreover, Tricetin suppressed the indicative protease, presenilin-1 (PS-1), as indicated by protease array. PS-1 was transcriptionally inhibited via the Akt signaling pathway but not mitogen-activated protein kinase pathways, such as the JNK, p38, and ERK1/2 pathways. In addition to upregulating GSK-3[Formula: see text] phosphorylation through Akt suppression, Tricetin may downregulate the activity of PS-1. Overall, our study provides new insight into the role of tricetin-induced molecular regulation in the suppression of NPC metastasis and suggests that Tricetin has prospective therapeutic applications for patients with NPC.
Tricetin Protects Rat Chondrocytes against IL-1 β-Induced Inflammation and Apoptosis
Oxid Med Cell Longev 2019 Apr 28;2019:4695381.PMID:31231454DOI:10.1155/2019/4695381.
Tricetin is a well-studied flavonoid with a wide range of pharmacological activities in cancer and inflammation. However, the ability of Tricetin to ameliorate the inflammation that occurs in osteoarthritis (OA) has not been determined. This study explored the effects of Tricetin on interleukin- (IL-) 1β-induced rat chondrocytes. Chondrocytes harvested from rat cartilage were incubated in vitro with Tricetin in the presence of IL-1β. The expression of matrix metalloproteinase- (MMP-) 1, MMP-3, MMP-13, nitric oxide (NO), prostaglandin E2 (PGE2), Bax, and Bcl-2 was evaluated by real-time-PCR, ELISA, Griess reaction, and western blotting. Caspase-3 activity in chondrocytes was determined using a caspase-3 activity assay and MAPK pathway activity by western blotting. Tricetin decreased the expression of MMP-1, MMP-3, and MMP-13 at both the gene and protein level in IL-1β-induced rat chondrocytes. It also inhibited IL-1β-induced NO and PGE2 production, by modulating inducible NO synthase and cyclooxygenase 2 gene expression. An antiapoptotic role of Tricetin involving the Bax/Bcl-2/caspase-3 pathway was also determined. The chondroprotective effect of Tricetin was shown to be partly related to the suppression of the MAPK signaling pathway. The results of this study demonstrate the chondroprotective role of Tricetin, based on its anticatabolic, anti-inflammatory, and antiapoptotic effects in chondrocytes. The therapeutic potential of Tricetin in OA patients should be explored in future studies.
Natural flavone Tricetin suppresses oxidized LDL-induced endothelial inflammation mediated by Egr-1
Int Immunopharmacol 2020 Mar;80:106224.PMID:31991371DOI:10.1016/j.intimp.2020.106224.
Atherosclerosis is the primary cause of many cardiovascular diseases. Endothelial dysfunction is recognized as a crucial early event in atherosclerotic lesion formation. Tricetin is a natural flavonoid derivative that has demonstrated a wide range of therapeutic properties. This study investigates the protective effect of Tricetin in cultured endothelial cells. The results of our study show that Tricetin suppressed oxidized low-density lipoprotein (ox-LDL)-induced expression of pro-inflammatory monocyte chemotactic protein-1 (MCP-1) and interleukin-1β (IL-1β), as well as the generation of reactive oxygen species (ROS). Furthermore, our findings indicate that Tricetin suppressed ox-LDL-induced expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). At the cellular level, the presence of Tricetin inhibited ox-LDL-induced monocyte adhesion to endothelial cells. Mechanistically, we showed that Tricetin suppressed the induction of the endothelial receptor for ox-LDL, lectin-like ox-LDL receptor-1 (LOX-1), and the transcriptional factor early growth response 1 (Egr-1) as well as extracellular signal-regulated protein kinase 1 and 2 (ERK1/2) activation. These data demonstrate that Tricetin is a natural protective agent in vascular endothelial cells, indicating that Tricetin could have a potentially beneficial effect in the modulation of atherosclerosis.
Tricetin inhibits human osteosarcoma cells metastasis by transcriptionally repressing MMP-9 via p38 and Akt pathways
Environ Toxicol 2017 Aug;32(8):2032-2040.PMID:27860196DOI:10.1002/tox.22380.
Tricetin, a dietary flavonoid, has cytostatic properties and anti-metastasis activities in various cancer cells. However, the detailed impacts and underlying mechanisms of Tricetin on human osteosarcoma cell metastasis are still unclear. Here, the hypothesis that Tricetin possesses the anti-metastatic effects on human osteosarcoma cells was tested. The effects of Tricetin on cell viability, motility, migration, and invasion in human osteosarcoma U2OS and HOS cells were investigated. Gelatin zymography, western blotting, polymerase chain reaction (PCR), and the luciferase assay were used to further explore the underlying mechanisms involved in anti-metastatic effects in U2OS cells. Their results showed that Tricetin, up to 80 μM without cytotoxicity, attenuated U2OS and HOS cells motility, invasiveness, and migration by reducing matrix metalloproteinase (MMP)-9 enzyme activities. In U2OS cells, Tricetin decreased MMP-9 protein and mRNA expressions, which was confirmed by real-time PCR. Next, Tricetin reduced phosphorylation of p38 and Akt, but no effect on phosphorylation of ERK1/2 and JNK. In conclusion, Tricetin possesses the anti-metastatic activity of osteosarcoma cells by transcriptionally repressing MMP-9 via p38 and Akt signaling pathways. This may be potentially useful as anti-metastatic agents for osteosarcoma chemotherapy.
Tricetin Induces Apoptosis of Human Leukemic HL-60 Cells through a Reactive Oxygen Species-Mediated c-Jun N-Terminal Kinase Activation Pathway
Int J Mol Sci 2017 Jul 31;18(8):1667.PMID:28758971DOI:10.3390/ijms18081667.
Tricetin is a dietary flavonoid with cytostatic properties and antimetastatic activities in various solid tumors. The anticancer effect of Tricetin in nonsolid tumors remains unclear. Herein, the molecular mechanisms by which Tricetin exerts its anticancer effects on acute myeloid leukemia (AML) cells were investigated. Results showed that Tricetin inhibited cell viability in various types of AML cell lines. Tricetin induced morphological features of apoptosis such as chromatin condensation and phosphatidylserine (PS) externalization, and significantly activated proapoptotic signaling including caspase-8, -9, and -3 activation and poly(ADP-ribose) polymerase (PARP) cleavage in HL-60 AML cells. Of note, tricetin-induced cell growth inhibition was dramatically reversed by a pan caspase and caspase-8- and -9-specific inhibitors, suggesting that this compound mainly acts through a caspase-dependent pathway. Moreover, treatment of HL-60 cells with Tricetin induced sustained activation of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK), and inhibition of ERK and JNK by their specific inhibitors respectively promoted and abolished tricetin-induced cell apoptosis. Dichlorofluorescein (DCF) staining showed that intracellular reactive oxygen species (ROS) levels were higher in tricetin-treated HL-60 cells compared to the control group. Moreover, an ROS scavenger, N-acetylcysteine (NAC), reversed tricetin-induced JNK activation and subsequent cell apoptosis. In conclusion, our results indicated that Tricetin induced cell death of leukemic HL-60 cells through induction of intracellular oxidative stress following activation of a JNK-mediated apoptosis pathway. A combination of Tricetin and an ERK inhibitor may be a better strategy to enhance the anticancer activities of Tricetin in AML.