Chebulic acid
(Synonyms: 诃子次酸) 目录号 : GC35672
A phenol with diverse biological activities
Cas No.:23725-05-5
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
Chebulic acid is a phenol that has been found in T. chebular and has diverse biological activities.1,2,3 It reduces production of reactive oxygen species (ROS) in human umbilical vein endothelial cells (HUVECs) induced by glyceraldehyde-related advanced glycation end products (glycer-AGEs) when used at a concentration of 100 ?g/ml.1 Chebulic acid reduces glycer-AGE-induced adhesion of HUVECs to THP-1 monocytes. It induces Nrf2 nuclear translocation and glutathione (GSH) synthesis and inhibits glycer-AGE-induced collagen accumulation, a marker of fibrosis, in LX-2 hepatic stellate cells.2 In vivo, chebulic acid (25 and 50 mg/kg) increases serum insulin levels and reduces blood urea nitrogen levels, proteinuria, albuminuria, and serum glucose levels in a diabetic rat model of ischemia-reperfusion-induced nephropathy.3
1.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) 2.Koo, Y.-C., Pyo, M.C., Nam, M.-H., et al.Chebulic acid prevents hepatic fibrosis induced by advanced glycation end-products in LX-2 cell by modulating Nrf2 translocation via ERK pathwayToxicol. In Vitro348-15(2016) 3.Silawat, N., and Gupta, V.B.Chebulic acid attenuates ischemia reperfusion induced biochemical alteration in diabetic ratsPharm. Biol.51(1)23-29(2013)
| Cas No. | 23725-05-5 | SDF | |
| 别名 | 诃子次酸 | ||
| Canonical SMILES | O=C(O)[C@H]([C@@H](C1=C(O)C(O)=C(O)C=C12)[C@@H](C(O)=O)OC2=O)CC(O)=O | ||
| 分子式 | C14H12O11 | 分子量 | 356.24 |
| 溶解度 | DMSO: 260 mg/mL (729.85 mM) | 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 | 2.8071 mL | 14.0355 mL | 28.071 mL |
| 5 mM | 0.5614 mL | 2.8071 mL | 5.6142 mL |
| 10 mM | 0.2807 mL | 1.4035 mL | 2.8071 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。
Chebulic acid Prevents Hypoxia Insult via Nrf2/ARE Pathway in Ischemic Stroke
Nutrients 2022 Dec 19;14(24):5390.PMID:36558549DOI:10.3390/nu14245390.
Excessive reactive oxygen species (ROS) production contributes to brain ischemia/reperfusion (I/R) injury through many mechanisms including inflammation, apoptosis, and cellular necrosis. Chebulic acid (CA) isolated from Terminalia chebula has been found to have various biological effects, such as antioxidants. In this study, we investigated the mechanism of the anti-hypoxic neuroprotective effect of CA in vitro and in vivo. The results showed that CA could protect against oxygen-glucose deprivation/reoxygenation (OGD/R) induced neurotoxicity in SH-SY5Y cells, as evidenced by the enhancement of cell viability and improvement of total superoxide dismutase (T-SOD) in SH-SY5Y cells. CA also attenuated OGD/R-induced elevations of malondialdehyde (MDA) and ROS in SH-SY5Y cells. Nuclear factor-E2-related factor 2 (Nrf2) is one of the key regulators of endogenous antioxidant defense. CA acted as antioxidants indirectly by upregulating antioxidant-responsive-element (ARE) and Nrf2 nuclear translocation to relieve OGD/R-induced oxidative damage. Furthermore, the results showed that CA treatment resulted in a significant decrease in ischemic infarct volume and improved performance in the motor ability of mice 24 h after stroke. This study provides a new niche targeting drug to oppose ischemic stroke and reveals the promising potential of CA for the control of ischemic stroke in humans.
Chebulic acid derivatives from Balakata baccata and their antineuroinflammatory and antioxidant activities
Bioorg Chem 2021 Nov;116:105332.PMID:34509045DOI:10.1016/j.bioorg.2021.105332.
Sixteen Chebulic acid derivatives, including nine new (1-9) and seven known (10-16) ones, were isolated from an ethanol extract of the branches and leaves of Balakata baccata. The structures of the new compounds were elucidated by their UV, IR, HRESIMS, NMR, electronic circular dichroism (ECD) and single-crystal X-ray diffraction data. The effects of all the isolates on antineuroinflammatory and antioxidant activities were evaluated. Compared with the positive control minocycline (IC50 = 1.21 ± 0.71 μM), compounds 1-16 with IC50 values being greater than 50 μM, displayed almost no effects on the inhibition of NO production in LPS-induced BV-2 microglial cells, however, the results of antioxidant activity for compounds 1-16 showed significant DPPH-radical scavenging abilities with EC50 value ranging from 3.98 to 14.24 μM, while the EC50 value of positive control vitamin C was 14.31 μM. At last, the results of PCR (qRT-PCR) analysis showed that compound 1 could enhance the expression of antioxidases (HO-1, GCLC, and NQO1) at the mRNA levels.
Chebulic acid Prevents Methylglyoxal-Induced Mitochondrial Dysfunction in INS-1 Pancreatic β-Cells
Antioxidants (Basel) 2020 Aug 20;9(9):771.PMID:32825285DOI:10.3390/antiox9090771.
To investigate the anti-diabetic properties of Chebulic acid (CA) associated with the prevention of methyl glyoxal (MG)-induced mitochondrial dysfunction in INS-1 pancreatic β-cells, INS-1 cells were pre-treated with CA (0.5, 1.0, and 2.0 μM) for 48 h and then treated with 2 mM MG for 8 h. The effects of CA and MG on INS-1 cells were evaluated using the following: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay; glyoxalase 1 (Glo-1) expression via Western blot and enzyme activity assays; Nrf-2, nuclear factor erythroid 2-related factor 2 protein expression via Western blot assay; reactive oxygen species (ROS) production assay; mRNA expression of mitochondrial dysfunction related components (UCP2, uncoupling protein 2; VDAC1, voltage-dependent anion-selective channel-1; cyt c, cytochrome c via quantitative reverse transcriptase-PCR; mitochondrial membrane potential (MMP); adenosine triphosphate (ATP) synthesis; glucose-stimulated insulin secretion (GSIS) assay. The viability of INS-1 cells was maintained upon pre-treating with CA before exposure to MG. CA upregulated Glo-1 protein expression and enzyme activity in INS-1 cells and prevented MG-induced ROS production. Mitochondrial dysfunction was alleviated by CA pretreatment; this occurred via the downregulation of UCP2, VDAC1, and cyt c mRNA expression and the increase of MMP and ATP synthesis. Further, CA pre-treatment promoted the recovery from MG-induced decrease in GSIS. These results indicated that CA could be employed as a therapeutic agent in diabetes due to its ability to prevent MG-induced development of insulin sensitivity and oxidative stress-induced dysfunction of β-cells.
Chebulic acid prevents hepatic fibrosis induced by advanced glycation end-products in LX-2 cell by modulating Nrf2 translocation via ERK pathway
Toxicol In Vitro 2016 Aug;34:8-15.PMID:27021876DOI:10.1016/j.tiv.2016.03.013.
Advanced glycation end-products (AGEs) are formed during normal aging, and at an accelerated rate in metabolic syndrome patients. Nonalcoholic steatohepatitis (NASH) can be caused by the AGEs in plasma, while glyceraldehyde-derived AGEs (glycer-AGEs) are significantly higher in the serum of NASH patients. In this study, we investigated the molecular mechanisms of Chebulic acid, isolated from Terminalia chebula Retz., in the inhibition of glycer-AGEs induced production of reactive oxygen species (ROS) and collagen accumulation using the LX-2 cell line. Chebulic acid significantly inhibited the induction of ROS and accumulation of collagen proteins by glycer-AGEs. ERK phosphorylation and total nuclear factor E2-related factor 2 (Nrf2) protein expression were induced by Chebulic acid in a dose-dependent manner. Chebulic acid was also found to induce translocation of Nrf2 into the nucleus, which was attenuated by inhibition of ERK phosphorylation through treatment with PD98059. Following translocation of Nrf2, Chebulic acid induced the protein expressions of catalytic subunit of γ-glutamylcysteine synthetase and glutathione synthesis. Collagen accumulation was also significantly reduced by Chebulic acid treatment. The observed effects of Chebulic acid were all inhibited by PD98059 treatment. Taken together, these results suggest that Chebulic acid prevents the glycer-AGEs-induced ROS formation of LX-2 cells and collagen accumulation by ERK-phosphorylation-mediated Nrf2 nuclear translocation, which causes upregulation of antioxidant protein production.
Chebulic acid attenuates ischemia reperfusion induced biochemical alteration in diabetic rats
Pharm Biol 2013 Jan;51(1):23-9.PMID:22963650DOI:10.3109/13880209.2012.698288.
Context: Diabetic nephropathy is one of the important microvascular complications of diabetes; however, the main problem remains is the control of progression of nephropathy in diabetes. Chebulic acid was selected, as tannins from Terminalia chebula are used as antidiabetic, renoprotective, antioxidant, hypotensive and an α-glucosidase inhibitor. Objective: In this study, we evaluated the effect of Chebulic acid on ischemia reperfusion induced biochemical alteration in diabetic rats. Materials and methods: Chebulic acid (CA) was isolated from T. chebula; LD(50) and acute toxicity studies of CA were done. Renal ischemia and reperfusion technique was used to induce nephropathy in diabetic rats. Glibenclamide (10 mg/kg) was used as diabetic standard; CA at doses of 25 and 50 mg/kg were administered for 28 days and various biochemical parameters were monitored. Results: The LD(50) was found to be 251 mg/kg; 25 and 50 mg/kg doses were selected as no toxic symptoms were observed at both doses, except slight diarrhea. CA significantly (p < 0.001) reduced the glucose, creatinine, urea nitrogen, glycosylated hemoglobulin, proteinuria, urine albumin excretion, glomerular filtration rate (GFR), and increased serum insulin and glycogen level. CA also restored glucose 6-phosphate dehydrogenase, glutathione, superoxide dismutase, catalase and malondialdehyde levels. Improvement in kidney was also noted in histopathological studies. Conclusions: The statistical data indicated that Chebulic acid at both doses (25 and 50 mg/kg) improves biochemical alterations caused by renal ischemia in diabetic rats.