Trilobatin
(Synonyms: 三叶苷) 目录号 : GC41374
A dihydrochalcone glucoside with diverse biological activities
Cas No.:4192-90-9
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Trilobatin is a dihydrochalcone glucoside and derivative of phloretin that has been found in Rooibos (A. linearis) tea and has diverse biological activities. It reduces survival of Bel 7402 and HepG2 cancer cells when used at a concentration of 100 μM. Trilobatin increases superoxide dismutase (SOD) and glutathione peroxidase (GPX) activity (EC50s = 129 and 128 μM, respectively) and inhibits lipid peroxidation (IC50 = 88 μM) in rat liver homogenates. Pretreatment with trilobatin reduces hydrogen peroxide-induced cell death and production of mitochondrial reactive oxygen species (ROS), prevents reduction in the mitochondrial membrane potential, and increases the activity of GPX, SOD2, and isocitrate dehydrogenase 2 (IDH2) in PC12 neuronal cells. Trilobatin inhibits infection by various HIV-1 strains (IC50s = 2.91-27.11 μM) without inducing cytotoxicity in target cells.
| Cas No. | 4192-90-9 | SDF | |
| 别名 | 三叶苷 | ||
| Canonical SMILES | OC1=CC=C(CCC(C2=C(O)C=C(O[C@@H]3O[C@H](CO)[C@@H](O)[C@H](O)[C@H]3O)C=C2O)=O)C=C1 | ||
| 分子式 | C21H24O10 | 分子量 | 436.4 |
| 溶解度 | DMF: 20 mg/ml,DMSO: 25 mg/ml,Ethanol: 20 mg/ml,PBS (pH 7.2): 0.1 mg/ml | 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 | 2.2915 mL | 11.4574 mL | 22.9148 mL |
| 5 mM | 0.4583 mL | 2.2915 mL | 4.583 mL |
| 10 mM | 0.2291 mL | 1.1457 mL | 2.2915 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。
Trilobatin rescues cognitive impairment of Alzheimer's disease by targeting HMGB1 through mediating SIRT3/SOD2 signaling pathway
Acta Pharmacol Sin 2022 Oct;43(10):2482-2494.PMID:PMC9525711DOI:10.1038/s41401-022-00888-5.
Alzheimer's disease (AD) is a progressive neurodegenerative disorder with cognitive impairment that currently is uncurable. Previous study shows that Trilobatin (TLB), a naturally occurring food additive, exerts neuroprotective effect in experimental models of AD. In the present study we investigated the molecular mechanisms underlying the beneficial effect of TLB on experimental models of AD in vivo and in vitro. APP/PS1 transgenic mice were administered TLB (4, 8 mg· kg-1 ·d-1, i.g.) for 3 months; rats were subjected to ICV injection of Aβ25-35, followed by administration of TLB (2.5, 5, 10 mg· kg-1 ·d-1, i.g.) for 14 days. We showed that TLB administration significantly and dose-dependently ameliorated the cognitive deficits in the two AD animal models, assessed in open field test, novel object recognition test, Y-maze test and Morris water maze test. Furthermore, TLB administration dose-dependently inhibited microglia and astrocyte activation in the hippocampus of APP/PS1 transgenic mice accompanied by decreased expression of high-mobility group box 1 (HMGB1), TLR4 and NF-κB. In Aβ25-25-treated BV2 cells, TLB (12.5-50 μM) concentration-dependently increased the cell viability through inhibiting HMGB1/TLR4/NF-κB signaling pathway. HMGB1 overexpression abrogated the beneficial effects of TLB on BV2 cells after Aβ25-35 insults. Molecular docking and surface plasmon resonance assay revealed that TLB directly bound to HMGB1 with a KD value of 8.541×10-4 M. Furthermore, we demonstrated that TLB inhibited Aβ25-35-induced acetylation of HMGB1 through activating SIRT3/SOD2 signaling pathway, thereby restoring redox homeostasis and suppressing neuroinflammation. These results, for the first time, unravel a new property of TLB: rescuing cognitive impairment of AD via targeting HMGB1 and activating SIRT3/SOD2 signaling pathway.
Trilobatin promotes angiogenesis after cerebral ischemia-reperfusion injury via SIRT7/VEGFA signaling pathway in rats
Phytother Res 2022 Jul;36(7):2940-2951.PMID:35537702DOI:10.1002/ptr.7487.
Angiogenesis plays a pivotal role in the recovery of neurological function after ischemia stroke. Herein, we investigated the effect of Trilobatin (TLB) on angiogenesis after cerebral ischemia-reperfusion injury (CIRI). The effect of TLB on angiogenesis after CIRI were investigated in mouse brain microvascular endothelium bEnd.3 cells and middle cerebral artery occlusion (MCAO)-induced CIRI rat model. The cell proliferation and angiogenesis were observed using immunofluorescence staining. The cell cycle, expressions of cell cycle-related proteins and SIRT 1-7 were determined by flow cytometry and western blot, respectively. The binding affinity of TLB with SIRT7 was predicted by molecular docking. The results showed that TLB concentration-dependently promoted bEnd.3 cell proportion in the S-phase. TLB significantly increased the protein expressions of SIRT6, SIRT7, and VEGFA, but not affected SIRT1-SIRT5 protein expressions. Moreover, TLB not only dramatically alleviated neurological impairment after CIRI, but also enhanced post-stroke neovascularization and newly formed functional vessels in cerebral ischemic penumbra. Furthermore, TLB up-regulated the protein expressions of CDK4, cyclin D1, VEGFA and its receptor VEGFR-2. Intriguingly, TLB not only directly bound to SIRT7, but also increased SIRT7 expression at day 28. Our findings reveal that TLB promotes cerebral microvascular endothelial cells proliferation, and facilitates angiogenesis after CIRI via mediating SIRT7/VEGFA signaling pathway in rats. Therefore, TLB might be a novel restorative agent to rescue ischemia stroke.
Trilobatin Induces Apoptosis and Attenuates Stemness Phenotype of Acquired Gefitinib Resistant Lung Cancer Cells via Suppression of NF-κB Pathway
Nutr Cancer 2022;74(2):735-746.PMID:33860693DOI:10.1080/01635581.2021.1912368.
Trilobatin is a common type of flavonoids compounds derived from Lithocarpus polystachyus Rehd leaves. Previous report suggests that Trilobatin was potentially involved in pro-and anticancer, antioxidative and anti-hyperglycemic activities. Here, we investigated the anticancer efficiency of Trilobatin on gefitinib resistant lung cancer cells. In this study, MTT assays, EdU incorporation assays, DAPI staining, tumor sphere formation assays, immunofluorescent staining and Western blot analysis were performed to explore the functional role of Trilobatin on gefitinib resistant lung cancer cells. The results showed that Trilobatin inhibits proliferation of gefitinib resistant lung cancer cells. In addition, the proportions of apoptotic cells were increased along with down-regulated expression levels of Bcl-2 and mitochondrial Cytochrome C while up-regulated Bax, Cleaved Caspase-3, -9, and cytosolic Cytochrome C expression. Moreover, Trilobatin decreased tumor sphere formation and expression levels of multiple stemness markers (ALDH1, CD133, Nanog, and ABCG2) in gefitinib resistant lung cancer cells. Furthermore, investigation of the mechanism indicated that Trilobatin suppressed activity of NF-κB via decreasing constitutive phosphorylation of NF-κB p65 and IκB-α in gefitinib resistant lung cancer cells. All these results indicate that Trilobatin induces apoptosis and attenuates stemness phenotype of gefitinib resistant lung cancer cells, involved with, or partly, the suppression of NF-κB activity.
Trilobatin alleviates non-alcoholic fatty liver disease in high-fat diet plus streptozotocin-induced diabetic mice by suppressing NLRP3 inflammasome activation
Eur J Pharmacol 2022 Oct 15;933:175291.PMID:36150533DOI:10.1016/j.ejphar.2022.175291.
Diabetes mellitus (DM) is a factor with great risk in the course of non-alcoholic fatty liver disease (NAFLD) due to its high glucotoxicity and lipotoxicity. Trilobatin, a glycosylated dihydrochalcone derived from the leaves of the Chinese sweet tea Lithocarpus polystachyus Rehd, is reported to possess various pharmacological activities. Nevertheless, it is still unclear regarding if Trilobatin can alleviate liver injury in diabetic mice with NAFLD and its mechanism. Our aim was to investigative the protective effects of Trilobatin against DM with NAFLD and its mechanism of action. A DM mice model was established by high-fat diet (HFD) feeding with streptozocin (STZ) injections, and treated with Trilobatin for 10 weeks. The biochemical results showed that Trilobatin restored glucose metabolic disorder and liver function in diabetic mice. The histopathological evaluation revealed that Trilobatin improved liver injury by alleviating lipid accumulation and liver fibrosis. Mechanistically, Trilobatin decreased expression of NLRP3, p65 NF-κB, cleaved-Caspase-1 and N-GSDMD, as well as the release of IL-18 and IL-1β, leading to a alleviation of inflammation and pyroptosis. Taken together, we determined for the first time found that Trilobatin could prevent liver injury in diabetic mice with NAFLD by suppressing NLRP3 inflammasome activation to reduce inflammation and pyroptosis.
Trilobatin, a Novel SGLT1/2 Inhibitor, Selectively Induces the Proliferation of Human Hepatoblastoma Cells
Molecules 2019 Sep 18;24(18):3390.PMID:31540429DOI:10.3390/molecules24183390.
Studies have indicated that Na+-d-glucose co-transporter (SGLT) inhibitors had anti-proliferative activity by attenuating the uptake of glucose in several tumor cell lines. In this study, the molecular docking showed that, Trilobatin, one of the dihydrochalcones from leaves of Lithocarpus polystachyus Rehd., might be a novel inhibitor of SGLT1 and SGLT2, which evidently attenuated the uptake of glucose in vitro and in vivo. To our surprise, we observed that Trilobatin did not inhibit, but promoted the proliferation of human hepatoblastoma HepG2 and Huh 7 cells when it was present at high concentrations. At the same time, incubation with high concentrations of Trilobatin arrested the cell cycle at S phase in HepG2 cells. We also found that treatment with Trilobatin had no significant effect on the expression of hepatitis B x-interacting protein (HBXIP) and hepatocyte nuclear factor (HNF)-4α, the two key regulators of hepatocyte proliferation. Taken together, although Trilobatin worked as a novel inhibitor of SGLTs to attenuate the uptake of glucose, it also selectively induced the cell proliferation of HepG2 cells, suggesting that not all the SGLT inhibitors inhibited the proliferation of tumor cells, and further studies are needed to assess the anti-cancer potentials of new glucose-lowering agents.