Hexahydrocurcumin
(Synonyms: 六氢姜黄素) 目录号 : GC34116
A natural product and an active metabolite of curcumin
Cas No.:36062-05-2
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Hexahydrocurcumin is a natural product and an active metabolite of curcumin.1 It reduces prostaglandin E2 (PGE2) production stimulated by phorbol 12-myristate 13-acetate by 37% in human colonic epithelial cells when used at a concentration of 20 ?M. Hexahydrocurcumin (3.125-25 ?M) inhibits overproduction of nitric oxide induced by LPS in RAW 264.7 macrophage cells in a concentration-dependent manner.2 It does not affect LPS-induced cytokine release but inhibits LPS-induced iNOS and COX-2 upregulation and NF-κB activation when used at a concentration of 50 ?M. Hexahydrocurcumin prevents the formation of aberrant crypt foci in a dimethylhydrazine rat model of colon cancer and potentiates the effect of 5-fluorouracil .3
1.Ireson, C., Orr, S., Jones, D.J., et al.Characterization of metabolites of the chemopreventive agent curcumin in human and rat hepatocytes and in the rat in vivo, and evaluation of their ability to inhibit phorbol ester-induced prostaglandin E2 productionCancer Res.61(3)1058-1064(2001) 2.Zhao, F., Gong, Y., Hu, Y., et al.Curcumin and its major metabolites inhibit the inflammatory response induced by lipopolysaccharide: Translocation of nuclear factor-κB as potential targetMol. Med. Rep.11(4)3087-3093(2015) 3.Srimuangwong, K., Tocharus, C., Tocharus, J., et al.Effects of hexahydrocurcumin in combination with 5-fluorouracil on dimethylhydrazine-induced colon cancer in ratsWorld J. Gastroenterol.18(47)6951-6959(2012)
| Cas No. | 36062-05-2 | SDF | |
| 别名 | 六氢姜黄素 | ||
| Canonical SMILES | O=C(CC(O)CCC1=CC=C(O)C(OC)=C1)CCC2=CC=C(O)C(OC)=C2 | ||
| 分子式 | C21H26O6 | 分子量 | 374.43 |
| 溶解度 | DMSO : 50 mg/mL (133.54 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 | 2.6707 mL | 13.3536 mL | 26.7073 mL |
| 5 mM | 0.5341 mL | 2.6707 mL | 5.3415 mL |
| 10 mM | 0.2671 mL | 1.3354 mL | 2.6707 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。
Hexahydrocurcumin ameliorates hypertensive and vascular remodeling in L-NAME-induced rats
Biochim Biophys Acta Mol Basis Dis 2022 Mar 1;1868(3):166317.PMID:34883248DOI:10.1016/j.bbadis.2021.166317.
Hexahydrocurcumin (HHC), a major metabolite of curcumin, possesses several biological activities such as antioxidant, anti-inflammation, and cardioprotective properties. This study aimed to investigate the effect of HHC on high blood pressure, vascular dysfunction, and remodeling induced by N-nitro L-arginine methyl ester (L-NAME) in rats. Male Wistar rats (200-250 g) received L-NAME (40 mg/kg) via drinking water for seven weeks. HHC at doses of 20, 40 or 80 mg/kg or enalapril 10 mg/kg was orally administered for the last three weeks. Blood pressure was measured weekly. Rats induced with L-NAME showed the development of hypertension, vascular dysfunction, and remodeling as demonstrated by an increase in wall thickness, cross-sectional area, and collagen deposition in the aorta. The overexpression of nuclear factor kappa B (NF-кB), vascular cell adhesion molecule 1 (VCAM1), intercellular adhesion molecule 1 (ICAM1), tumor necrosis factor-alpha (TNF-α), phosphorylated-extracellular-regulated kinase 1/2 (p-ERK1/2), phosphorylated-c-Jun N-terminal kinases (p-JNK), phosphorylated-mitogen activated protein kinase p38 (p-p38), transforming growth factor-beta 1 (TGF-β1), matrix metalloproteinase-9 (MMP-9) and collagen type 1 was observed in L-NAME-induced hypertensive rats. Increased oxidative stress markers, decreased plasma nitric oxide (NO) levels and the down-regulation of endothelial nitric oxide synthase (eNOS) expression in aortic tissues were also found in L-NAME-induced rats. Moreover, L-NAME-induced rats showed enhanced synthetic protein expression in aortic tissues. These alterations were suppressed in hypertensive rats treated with HHC or enalapril. The present study shows that HHC exhibited antihypertensive effects by improving vascular function and ameliorated the development of vascular remodeling. The responsible mechanism may involve antioxidant and anti-inflammation potential.
Biological and pharmacological effects of Hexahydrocurcumin, a metabolite of curcumin
Arch Biochem Biophys 2018 May 15;646:31-37.PMID:29596797DOI:10.1016/j.abb.2018.03.030.
Curcumin, one of the most precious pharmacologically relevant natural products, has gained considerable attention among scientists for decades because of its multi-pharmacological activities in the clinical. However, critical studies on its pharmacological and toxicological activities are needed to understand how this compound can have these biological functions considering its poor oral bioavailability and the low plasma concentration. Moreover, curcumin undergoes extensive and rapid metabolism in vivo, indicating that the pharmacological activity of consuming curcumin might be mediated partly by its metabolites. And as one of the major curcumin metabolites, Hexahydrocurcumin (HHC), exhibits similar or more potent bioactivity than curcumin by in vitro and in vivo studies, such as antioxidant, anti-inflammatory, antitumor and cardiovascular protective properties, which may provide important information for us to have a profound comprehension of the effectiveness of curcumin. This review mainly summarizes the current knowledge and underlying molecular mechanisms of the biological activities of HHC and its potential effects on the development of various human diseases.
Inhibitory Effect of Hexahydrocurcumin on Memory Impairment and Amyloidogenesis in Dexamethasone-Treated Mice
Neurotox Res 2021 Apr;39(2):266-276.PMID:32852718DOI:10.1007/s12640-020-00269-y.
A high dose of dexamethasone induces neurodegeneration by initiating the inflammatory processes that lead to neural apoptosis. A dexamethasone administration model induces overproduction of amyloid-β (Aβ) and tau protein hyperphosphorylation and shows abnormalities of cholinergic function similar to Alzheimer's disease (AD). This study aimed to investigate the protective effect of Hexahydrocurcumin on the brain of dexamethasone-induced mice. The results showed that Hexahydrocurcumin and donepezil attenuated the levels of amyloid precursor protein and β-secretase mRNA by reverse transcription polymerase chain reaction, decreased the expression of hyperphosphorylated tau, and improved synaptic function. Moreover, we found that Hexahydrocurcumin treatment could decrease interleukin-6 levels by attenuating p65 of nuclear factor kappa-light-chain-enhancer (NF-κB) of activated beta cells. In addition, Hexahydrocurcumin also decreased oxidative stress, as demonstrated by the expression of 4-hydroxynonenal and thereby prevented apoptosis. Therefore, our finding suggests that Hexahydrocurcumin prevents dexamethasone-induced AD-like pathology and improves memory impairment.
Production of Optically Active Hexahydrocurcumin by Human Intestinal Bacterium in Vitro
Biol Pharm Bull 2021;44(1):136-139.PMID:33390541DOI:10.1248/bpb.b20-00584.
A hexahydrocurcumin-producing bacterium named 2a1-2b was isolated from human feces. It was observed that the bacterium had more than 99% similarity with Enterococcus avium ATCC14025T according to 16S ribosomal DNA (rDNA) sequence. The strain 2a1-2b produced optically active 5R-hexahydrocurcumin (enantiomeric excess (e.e.) > 95%) from tetrahydrocurcumin but not from curcumin. Our results showed that intestine is an important place for producing Hexahydrocurcumin.
Hexahydrocurcumin alleviated blood-brain barrier dysfunction in cerebral ischemia/reperfusion rats
Pharmacol Rep 2020 Jun;72(3):659-671.PMID:32048258DOI:10.1007/s43440-019-00050-9.
Background: Hexahydrocurcumin (HHC), a major metabolite of curcumin, has been reported to have protective effects against ischemic and reperfusion damage. The goal of the present research was to examine whether HHC could alleviate brain damage and ameliorate functional outcomes by diminishing the blood-brain barrier (BBB) damage that follows cerebral ischemia/reperfusion. Methods: Middle cerebral artery occlusion was induced for 2 h in rats followed by reperfusion. The rats were divided into three groups: sham-operated, vehicle-treated, and HHC-treated groups. At the onset of reperfusion, the rats were immediately intraperitoneally injected with 40 mg/kg HHC. At 48 h after reperfusion, the rats were evaluated for neurological deficits and TTC staining. At 24 h and 48 h after reperfusion, animals were sacrificed, and their brains were extracted. Results: Treatment with HHC reduced neurological scores, infarct volume, morphological changes, Evans blue leakage and immunoglobulin G extravasation. Moreover, HHC treatment reduced BBB damage and neutrophil infiltration, downregulated myeloperoxidase, ICAM-1, and VCAM-1, upregulated tight junction proteins (TJPs), and reduced aquaporin 4 expression and brain water content. Conclusion: These results revealed that HHC treatment preserved the BBB from cerebral ischemia/reperfusion injury by regulating TJPs, attenuating neutrophil infiltration, and reducing brain edema formation.