Tricin
(Synonyms: 苜蓿素) 目录号 : GC39158
Tricin 是米糠中大量存在的一种天然类黄酮。Tricin 通过抑制 CDK9 来抑制 HCMV 的复制。Tricin 通过上调 FAK 靶向 microRNA-7 的表达来抑制 C6 胶质瘤细胞的增殖和侵袭。
Cas No.:520-32-1
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Tricin is a natural flavonoid present in large amounts in rice bran. Tricin can inhibit human cytomegalovirus (HCMV) replication by inhibiting CDK9. Tricin inhibits the proliferation and invasion of C6 glioma cells via the upregulation of focal-adhesion-finase (FAK)-targeting microRNA-7[1][2][3].
[1]. Itoh A, et al. Tricin inhibits the CCL5 induction required for efficient growth of human cytomegalovirus. Microbiol Immunol. 2018 May;62(5):341-347. [2]. Sadanari H, et al. The anti-human cytomegalovirus drug tricin inhibits cyclin-dependent kinase 9. FEBS Open Bio. 2018 Feb 20;8(4):646-654. [3]. Chung DJ, et al. Inhibition of the Proliferation and Invasion of C6 Glioma Cells by Tricin via the Upregulation of Focal-Adhesion-Kinase-Targeting MicroRNA-7. J Agric Food Chem. 2018 Jul 5;66(26):6708-6716.
| Cas No. | 520-32-1 | SDF | |
| 别名 | 苜蓿素 | ||
| Canonical SMILES | O=C1C=C(C2=CC(OC)=C(O)C(OC)=C2)OC3=CC(O)=CC(O)=C13 | ||
| 分子式 | C17H14O7 | 分子量 | 330.29 |
| 溶解度 | DMSO: 125 mg/mL (378.46 mM) | 储存条件 | 4°C, protect from light |
| 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 | 3.0276 mL | 15.1382 mL | 30.2764 mL |
| 5 mM | 0.6055 mL | 3.0276 mL | 6.0553 mL |
| 10 mM | 0.3028 mL | 1.5138 mL | 3.0276 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
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。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Tricin Biosynthesis and Bioengineering
Front Plant Sci 2021 Aug 26;12:733198.PMID:34512707DOI:10.3389/fpls.2021.733198.
Tricin (3',5'-dimethoxyflavone) is a specialized metabolite which not only confers stress tolerance and involves in defense responses in plants but also represents a promising nutraceutical. Tricin-type metabolites are widely present as soluble Tricin O-glycosides and tricin-oligolignols in all grass species examined, but only show patchy occurrences in unrelated lineages in dicots. More strikingly, Tricin is a lignin monomer in grasses and several other angiosperm species, representing one of the "non-monolignol" lignin monomers identified in nature. The unique biological functions of Tricin especially as a lignin monomer have driven the identification and characterization of Tricin biosynthetic enzymes in the past decade. This review summarizes the current understanding of Tricin biosynthetic pathway in grasses and tricin-accumulating dicots. The characterized and potential enzymes involved in Tricin biosynthesis are highlighted along with discussion on the debatable and uncharacterized steps. Finally, current developments of bioengineering on manipulating Tricin biosynthesis toward the generation of functional food as well as modifications of lignin for improving biorefinery applications are summarized.
Metabolomics and integrated network pharmacology analysis reveal Tricin as the active anti-cancer component of Weijing decoction by suppression of PRKCA and sphingolipid signaling
Pharmacol Res 2021 Sep;171:105574.PMID:34419228DOI:10.1016/j.phrs.2021.105574.
Currently, conventional methods of treating non-small cell lung cancer (NSCLC) have many disadvantages. An alternative effective therapy with minimal adverse reactions is urgently needed. Weijing decoction (WJD), which is a classic ancient Chinese herbal prescription, has been used successfully to treat pulmonary system diseases containing lung cancer in the clinic. However, the key active component and target of Weijing decoction are still unexplored. Therefore, for the first time, our study aims to investigate the pharmacological treatment mechanism of Weijing decoction in treating NSCLC via an integrated model of network pharmacology, metabolomics and biological methods. Network pharmacology results conjectured that Tricin is a main bioactive component in this formula which targets PRKCA to suppress cancer cell growth. Metabolomics analysis demonstrated that sphingosine-1-phosphate, which is regulated by sphingosine kinase 1 and sphingosine kinase 2, is a differential metabolite in plasma between the WJD-treated group and the control group, participating in the sphingolipid signaling. In vitro experiments demonstrated that Tricin had vital effects on the proliferation, pro-apoptosis, migration and colony formation of Lewis lung carcinoma cells. Through a series of validation assays, Tricin inhibited the tumor growth mainly by suppressing PRKCA/SPHK/S1P signaling and antiapoptotic signaling. On the other hand, Weijing formula could inhibit the tumor growth and prolong the survival time. A high dosage of Tricin was much more potent in animal experiments. In conclusion, we confirmed that Weijing formula and its primary active compound Tricin are promising alternative treatments for NSCLC patients.
A flavonoid monomer Tricin in Gramineous plants: Metabolism, bio/chemosynthesis, biological properties, and toxicology
Food Chem 2020 Aug 1;320:126617.PMID:32247167DOI:10.1016/j.foodchem.2020.126617.
Tricin (5,7,4'-trihydroxy-3',5'-dimethoxyflavone) as a renewable and bioactive polyphenolic compound is widely distributed in monocots with free and conjugated forms. It is derived from the secondary metabolite of plants with an analogous biosynthetic pathway to other flavonoids. Due to its unique biological properties over other flavonoids, Tricin has been linked to numerous health benefits for human nutrition. In recent years, Tricin has been demonstrated to have excellent pharmacological bioactivities and has been proposed as a safe candidate for cancer chemoprevention. For throwing light on the structure-activity relationship of Tricin monomer and its potential clinical application, the natural occurrence, physicochemical characteristics, bio/chemosynthesis, isolation and purification, biological properties involved metabolism in vitro and in vivo of Tricin as well as its toxicology and bioavailability are critically reviewed, which aims at greatly moving forward the value-added applications of this natural bioactive material on food, human nutrition, and pharmacology.
Inhibiting Tricin biosynthesis improves maize lignocellulose saccharification
Plant Physiol Biochem 2022 May 1;178:12-19.PMID:35247693DOI:10.1016/j.plaphy.2022.02.018.
Lignin is a technological bottleneck to convert polysaccharides into fermentable sugars, and different strategies of genetic-based metabolic engineering have been applied to improve biomass saccharification. Using maize seedlings grown hydroponically for 24 h, we conducted a quick non-transgenic approach with five enzyme inhibitors of the lignin and Tricin pathways. Two compounds [3,4-(methylenedioxy)cinnamic acid: MDCA and 2,4-pyridinedicarboxylic acid: PDCA] revealed interesting findings on root growth, lignin composition, and saccharification. By inhibiting hydroxycinnamoyl-CoA ligase, a key enzyme of phenylpropanoid pathway, MDCA decreased the lignin content and improved saccharification, but it decreased root growth. By inhibiting flavone synthase, a key enzyme of Tricin biosynthesis, PDCA decreased total lignin content and improved saccharification without affecting root growth. PDCA was three-fold more effective than MDCA, suggesting that controlling lignin biosynthesis with enzymatic inhibitors may be an attractive strategy to improve biomass saccharification.
Tricin attenuates cerebral ischemia/reperfusion injury through inhibiting nerve cell autophagy, apoptosis and inflammation by regulating the PI3K/Akt pathway
Hum Exp Toxicol 2022 Jan-Dec;41:9603271221125928.PMID:36113040DOI:10.1177/09603271221125928.
To elucidate the effect of Tricin in cerebral ischemia/reperfusion (I/R) injury and examine its possible underlying mechanisms. Rats were randomly divided into Sham (exposed the right internal carotid arteries), I/R, and Tricin (administered at various doses) groups. After the cerebral I/R injury model was established, a Morris water maze test and a tetrazolium chloride assay were performed. Apoptosis and autophagy were assessed in the nerve cells of hippocampus tissue, and the levels of inflammatory markers within animal serum were detected. Proteins related to apoptosis and the PI3K/Akt pathway were evaluated. To further investigate the mechanisms by which Tricin affects brain damage, mouse neuroblastoma cells N2a were divided into control, oxygen-glucose deprivation and reoxygenation (OGD/R), Tricin, PI3K/Akt activator, and Tricin + PI3K/Akt inhibitor groups. The cell viability, apoptosis, inflammatory factors, and PI3K/Akt pathway related proteins in N2a cells were also detected. The results revealed that I/R-induced learning and memory dysfunction was improved by Tricin treatment. The area of cerebral infarction, the levels of apoptosis and autophagy in nerve cells, and the serum inflammatory marker content were all decreased following Tricin treatment. Additionally, the expression of Beclin-1 protein was downregulated, while the expression of Bcl-2 protein, p-PI3K/PI3K and p-Akt/Akt was upregulated after Tricin treatment. Mechanistically, Tricin or PI3K/Akt activator ameliorated OGD/R-induced apoptosis, autophagy, and inflammation. However, these effects were reversed following PI3K/Akt inhibitor treatment in OGD/R-induced N2a cells. In summary, this study suggested that Tricin can against I/R-induced brain injury by inhibiting autophagy, apoptosis and inflammation, and activating the PI3K/Akt signaling pathway.