Chebulinic acid
(Synonyms: 诃子林鞣酸) 目录号 : GC32250
An ellagitannin with diverse biological activities
Cas No.:18942-26-2
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Chebulinic acid is an ellagitannin that has been found in T. chebula and has diverse biological activities.1,2,3,4,5 It is an inhibitor of protein tyrosine phosphatase non-receptor 9 (PTPN9) and PTPN11 (IC50s = 34 and 37 nM, respectively).2 Chebulinic acid (5 ?M) increases glucose uptake in 3T3-L1 preadipocytes. It induces apoptosis of HL-60 and NB4 acute promyelocytic leukemia (APL), but not K562 chronic myelogenous leukemia (CML), cells (IC50s = 7.5, 5, and >60 ?M, respectively).1 Chebulinic acid (25 ?M) reduces the production of reactive oxygen species (ROS) induced by glyceraldehyde-related advanced glycation end products (glycer-AGEs) in human umbilical vein endothelial cells (HUVECs) and reduces glutamate-induced ROS production and cell death in HT22 mouse hippocampal cells.3,4 It inhibits H+/K+-ATPase activity (IC50 = 65.01 ?g/ml) and reduces free and total gastric acidity, as well as increases gastric mucin secretion, in various rat models of gastric ulcer.5
1.Chhabra, S., Mishra, T., Kumar, Y., et al.Chebulinic acid isolated from the fruits of Terminalia chebula specifically induces apoptosis in acute myeloid leukemia cellsPhytother. Res.31(12)1849-1857(2017) 2.Yoon, S.-Y., Kang, H.J., Ahn, D., et al.Identification of chebulinic acid as a dual targeting inhibitor of protein tyrosine phosphatases relevant to insulin resistanceBioorg. Chem.90103087(2019) 3.Lee, H.-S., Koo, Y.-C., Suh, H.J., et al.Preventive effects of chebulic acid isolated from Terminalia chebula on advanced glycation endproduct-induced endothelial cell dysfunctionJ. Ethnopharmacol.131(3)567-574(2010) 4.Song, J.H., Shin, M.-S., Hwang, G.S., et al.Chebulinic acid attenuates glutamate-induced HT22 cell death by inhibiting oxidative stress, calcium influx and MAPKs phosphorylationBioorg. Med. Chem. Lett.28(3)249-253(2018) 5.Mishra, V., Agrawal, M., Onasanwo, S.A., et al.Anti-secretory and cyto-protective effects of chebulinic acid isolated from the fruits of Terminalia chebula on gastric ulcersPhytomedicine20(6)506-511(2013)
| Cas No. | 18942-26-2 | SDF | |
| 别名 | 诃子林鞣酸 | ||
| Canonical SMILES | OC(C[C@H](C(O[C@@]([C@H](O[C@H]1OC(C2=CC(O)=C(O)C(O)=C2)=O)COC(C3=CC(O)=C(O)C(O)=C3)=O)([H])[C@@](OC(C4=CC(O)=C(O)C(O)=C4)=O)([H])[C@@]1([H])OC5=O)=O)[C@@]([C@H]6O)([H])C(C5=CC(O)=C7O)=C7OC6=O)=O | ||
| 分子式 | C41H32O27 | 分子量 | 956.68 |
| 溶解度 | Ethanol: soluble | 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 | 1.0453 mL | 5.2264 mL | 10.4528 mL |
| 5 mM | 0.2091 mL | 1.0453 mL | 2.0906 mL |
| 10 mM | 0.1045 mL | 0.5226 mL | 1.0453 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。
Chebulinic acid Suppresses Adipogenesis in 3T3-L1 Preadipocytes by Inhibiting PPP1CB Activity
Int J Mol Sci 2022 Jan 13;23(2):865.PMID:35055051DOI:10.3390/ijms23020865.
Depletion of protein phosphatase-1 catalytic subunit beta (PPP1CB), a serine/threonine protein phosphatase and potent adipogenic activator, suppresses the differentiation of 3T3-L1 preadipocytes into mature adipocytes. Therefore, PPP1CB is considered as a potential therapeutic target for obesity. We screened 1033 natural products for PPP1CB inhibitors and identified Chebulinic acid, which is abundantly present in the seeds of Euphoria longana and fruits of Terminalia chebula. Chebulinic acid strongly inhibited the hydrolysis of 6,8-difluoro-4-methylumbelliferyl phosphate by PPP1CB (IC50 = 300 nM) and demonstrated potent antiadipogenic effects in 3T3-L1 preadipocytes in a concentration-dependent manner. Additional studies have demonstrated that Chebulinic acid suppresses early differentiation by downregulating key transcription factors that control adipogenesis in 3T3-L1 cells. These results suggested that Chebulinic acid may be a potential therapeutic agent for treating obesity by inhibiting PPP1CB activity.
Ferroptosis-Inhibitory Difference between Chebulagic Acid and Chebulinic acid Indicates Beneficial Role of HHDP
Molecules 2021 Jul 15;26(14):4300.PMID:34299576DOI:10.3390/molecules26144300.
The search for a safe and effective inhibitor of ferroptosis, a recently described cell death pathway, has attracted increasing interest from scientists. Two hydrolyzable tannins, chebulagic acid and Chebulinic acid, were selected for the study. Their optimized conformations were calculated using computational chemistry at the B3LYP-D3(BJ)/6-31G and B3LYP-D3(BJ)/6-311 + G(d,p) levels. The results suggested that (1) chebulagic acid presented a chair conformation, while Chebulinic acid presented a skew-boat conformation; (2) the formation of chebulagic acid requires 762.1729 kcal/mol more molecular energy than Chebulinic acid; and (3) the 3,6-HHDP (hexahydroxydiphenoyl) moiety was shown to be in an (R)- absolute stereoconfiguration. Subsequently, the ferroptosis inhibition of both tannins was determined using a erastin-treated bone marrow-derived mesenchymal stem cells (bmMSCs) model and compared to that of ferrostatin-1 (Fer-1). The relative inhibitory levels decreased in the following order: Fer-1 > chebulagic acid > Chebulinic acid, as also revealed by the in vitro antioxidant assays. The UHPLC-ESI-Q-TOF-MS analysis suggested that, when treated with 16-(2-(14-carboxytetradecyl)-2-ethyl-4,4-dimethyl-3-oxazolidinyloxy free radicals, Fer-1 generated dimeric products, whereas the two acids did not. In conclusion, two hydrolyzable tannins, chebulagic acid and Chebulinic acid, can act as natural ferroptosis inhibitors. Their ferroptosis inhibition is mediated by regular antioxidant pathways (ROS scavenging and iron chelation), rather than the redox-based catalytic recycling pathway exhibited by Fer-1. Through antioxidant pathways, the HHDP moiety in chebulagic acid enables ferroptosis-inhibitory action of hydrolyzable tannins.
Chebulinic and chebulagic acid binding with serum proteins: biophysical and molecular docking approach
J Biomol Struct Dyn 2022 Apr 9;1-16.PMID:35403561DOI:10.1080/07391102.2022.2060862.
Chebulinic acid (CHN) and chebulagic acid (CHG) have been known for centuries for their anti-cancer, anti-diabetes, HIV and anti-inflammatory properties. In this study, the interaction of these phytochemicals CHN/CHG, with the two major transport proteins for various drugs, human serum albumin (HSA) and 伪-1-acid glycoprotein (AGP), was unraveled by using several spectroscopic techniques and computational methods. The binding of CHN/CHG quenches the HSA/AGP fluorescence intensities, and also these phytochemicals are bound strongly to HSA/AGP proteins. An apparent decrease in fluorescence intensities of CHN/CHG-HSA and CHN/CHG-AGP complex showed the static mode of fluorescence quenching. Furthermore, the intrinsic fluorescence and using site-specific markers ibuprofen competing with these molecules, thereby replacing it in the binding site of subdomain IIIA. The computational methods substantiated the experimental findings, revealing that CHN interacted with Lys414A, Glu492A, Glu492A and Lys413A residues of subdomain IIIA of HSA and for CHG showed the interaction with Lys545A and Lys413A residues of subdomain IIIA of HSA. Fluorescence and surface plasmon resonance data unveiled a previously unreported binding event between CHN/CHG and HSA; the determined binding affinities of both compounds were slightly higher for HSA than AGP. A change in functionality of protein confirmed the esterase-like activity of HSA in the presence of CHG/CHN upon binding with CHG/CHN. Displacement and circular dichroism (CD) experiments analysis showed that the two CHN/CHG and binding specifically to IIIA subdomain on HSA results in the conformational changes in the HSA. Thus, CD revealed a few conformational changes in HSA due to CHN/CHG. The binding of these two phytochemicals to the plasma proteins would give a path to develop new inspired drug molecules for chronic diseases.Communicated by Ramaswamy H. Sarma.
Chebulinic acid attenuates glutamate-induced HT22 cell death by inhibiting oxidative stress, calcium influx and MAPKs phosphorylation
Bioorg Med Chem Lett 2018 Feb 1;28(3):249-253.PMID:29317168DOI:10.1016/j.bmcl.2017.12.062.
Glutamate-induced excitotoxicity and oxidative stress is a major causative factor in neuronal cell death in acute brain injuries and chronic neurodegenerative diseases. The prevention of oxidative stress is a potential therapeutic strategy. Therefore, in the present study, we aimed to examine a potential therapeutic agent and its protective mechanism against glutamate-mediated cell death. We first found that Chebulinic acid isolated from extracts of the fruit of Terminalia chebula prevented glutamate-induced HT22 cell death. Chebulinic acid significantly reduced intracellular reactive oxygen species (ROS) production and Ca2+ influx induced by glutamate. We further demonstrated that Chebulinic acid significantly decreased the phosphorylation of mitogen-activated protein kinases (MAPKs), including ERK1/2, JNK, and p38, as well as inhibiting pro-apoptotic Bax and increasing anti-apoptotic Bcl-2 protein expression. Moreover, we demonstrated that Chebulinic acid significantly reduced the apoptosis induced by glutamate in HT22 cells. In conclusion, our results in this study suggest that Chebulinic acid is a potent protectant against glutamate-induced neuronal cell death via inhibiting ROS production, Ca2+ influx, and phosphorylation of MAPKs, as well as reducing the ratio of Bax to Bcl-2, which contribute to oxidative stress-mediated neuronal cell death.
Chebulinic acid Isolated From the Fruits of Terminalia chebula Specifically Induces Apoptosis in Acute Myeloid Leukemia Cells
Phytother Res 2017 Dec;31(12):1849-1857.PMID:28921713DOI:10.1002/ptr.5927.
Chebulinic acid, an ellagitannin found in the fruits of Terminalia chebula, has been extensively used in traditional Indian system of medicine. It has shown to have various biological activities including antitumor activity. The present study aims to investigate the cytotoxic potential of Chebulinic acid in human myeloid leukemia cells. Interestingly, Chebulinic acid caused apoptosis of acute promyelocytic leukemia HL-60 and NB4 cells but not K562 cells. In vitro antitumor effects of Chebulinic acid were investigated by using various acute myeloid leukemia cell lines. Chebulinic acid treatment to HL-60 and NB4 cells induced caspase activation, cleavage of poly(ADP-ribose) polymerase, DNA fragmentation, chromatin condensation, and changes in the mitochondrial membrane permeability. Additionally, inhibition of caspase activation drastically reduced the chebulinic acid-induced apoptosis of acute promyelocytic leukemia cells. Our data also demonstrate that chebulinic acid-induced apoptosis in HL-60 and NB4 cells involves activation of extracellular signal-regulated kinases, which, when inhibited with ERK inhibitor PD98059, mitigates the chebulinic acid-induced apoptosis. Taken together, our findings exhibit the selective potentiation of chebulinic acid-induced apoptosis in acute promyelocytic leukemia cells. Copyright 漏 2017 John Wiley & Sons, Ltd.