Kakkalide
(Synonyms: 葛花苷) 目录号 : GC36380
Kakkalide 是一种由葛根花提取的异黄酮。Kakkalide 能通过抑制活性氧 (ROS) 相关炎症来改善内皮细胞胰岛素抵抗作用。
Cas No.:58274-56-9
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
Kakkalide is an isoflavone derived from the flowers of Pueraria lobata. Kakkalide ameliorates endothelial insulin resistance by suppressing reactive oxygen species (ROS)-associated inflammation[1].
[1]. Zhang D, et al. Kakkalide ameliorates endothelial insulin resistance by suppressing reactive oxygen species-associated inflammation. J Diabetes. 2013 Mar;5(1):13-24.
| Cas No. | 58274-56-9 | SDF | |
| 别名 | 葛花苷 | ||
| Canonical SMILES | O=C1C2=C(O)C(OC)=C(O[C@@H]3O[C@@H]([C@@H](O)[C@H](O)[C@H]3O)CO[C@H]4[C@@H]([C@H]([C@H](O)CO4)O)O)C=C2OC=C1C5=CC=C(OC)C=C5 | ||
| 分子式 | C28H32O15 | 分子量 | 608.54 |
| 溶解度 | Soluble in DMSO | 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 | 1.6433 mL | 8.2164 mL | 16.4328 mL |
| 5 mM | 0.3287 mL | 1.6433 mL | 3.2866 mL |
| 10 mM | 0.1643 mL | 0.8216 mL | 1.6433 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。
Kakkalide ameliorates endothelial insulin resistance by suppressing reactive oxygen species-associated inflammation
J Diabetes 2013 Mar;5(1):13-24.PMID:23190749DOI:10.1111/1753-0407.12017.
Background: Kakkalide is the predominant isoflavone derived from the flowers of Pueraria lobata (Willd.) Ohwi. The aim of the present study was to investigate the effects of Kakkalide on insulin resistance in the endothelium. Methods: Human umbilical vein endothelial cells (HUVEC) were stimulated with 100 μmol/L palmitate (PA) for 30 min and the effects of 30 min pretreatment with 0.1-10 μmol/L Kakkalide on reactive oxygen species (ROS)-associated inflammation in cells were evaluated by western blot analysis and reverse transcription-polymerase chain reaction. Furthermore, we investigated the biomodulation of insulin signaling by Kakkalide along the insulin receptor substrate (IRS)-1/Akt/endothelial nitric oxide synthase (eNOS) pathway. We also determined the effects of 30 min pretreatment with 0.1-10 μmol/L Kakkalide on insulin-mediated endothelium-dependent vasodilation of rat aorta in vitro following stimulation with 100 μmol/L PA. Results: Kakkalide inhibited ROS overproduction and effectively restored mitochondrial membrane potential, demonstrating its chemoprotection of mitochondrial function. In addition, Kakkalide inhibited ROS-associated inflammation in the endothelium by inhibiting tumor necrosis factor-α and interleukin-6 production and gene expression, as well as suppressing the phosphorylation of c-Jun N-terminal kinase and IκB kinase β/nuclear factor-κB. Inflammation impaired insulin phosphatidylinositol 3-kinase (PI3K) signaling and reduced insulin-mediated NO production in endothelial cells. Kakkalide facilitated PI3K signaling by positively regulating serine/tyrosine phosphorylation of IRS-1. Conclusions: Kakkalide inhibited ROS-associated inflammation and ameliorated insulin-resistant endothelial dysfunction by beneficial effects on IRS-1 function.
Kakkalide and irisolidone alleviate 2,4,6-trinitrobenzenesulfonic acid-induced colitis in mice by inhibiting lipopolysaccharide binding to toll-like receptor-4 and proteobacteria population
Int Immunopharmacol 2019 Aug;73:246-253.PMID:31112869DOI:10.1016/j.intimp.2019.05.008.
The flower of Pueraria lobata (family Fabaceae) has been clinically used in traditional Chinese medicine to counteract symptoms associated with drinking alcohol and liver injury and to alleviate inflammatory diseases. Its major constituent Kakkalide is metabolized to irisolidone by gut microbiota. This research study was undertaken to understand the anti-colitis mechanism of Kakkalide and irisolidone in vitro and in vivo. Kakkalide and its metabolite irisolidone inhibited lipopolysaccharide (LPS)-stimulated NF-κB activation and TNF-α expression in macrophages. They also inhibited LPS-induced phosphorylation of IRAK1 and TAK1 and activation of NF-κB by inhibiting the binding of Alexa Fluor 488-conjugated LPS in vitro. Orally administered irisolidone or Kakkalide alleviated colon shortening and myeloperoxidase activity in mice with 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis. Their treatments also protected epithelial cell disruption and infiltration of CD11b+/CD11c+ cells in the colon. Furthermore, they suppressed TNBS-induced expression of M1 macrophage markers TNF-α, CD80, CD86, and Arg2 expression while the expression of M2 macrophage markers Arg1, CD163, CD206, and IL-10 was induced. They also suppressed the fecal Proteobacteria population. Overall, the anti-colitic effects of irisolidone were superior to those of Kakkalide. Kakkalide and its metabolite irisolidone inhibited inflammation in vitro and in vivo by inhibiting LPS binding to toll-like receptor 4 and gut proteobacteria population.
Kakkalide and its metabolite irisolidone ameliorate carrageenan-induced inflammation in mice by inhibiting NF-κB pathway
Inflammation 2011 Oct;34(5):344-51.PMID:20686830DOI:10.1007/s10753-010-9240-1.
The anti-inflammatory activities of Kakkalide, a major constituent of the flower of Pueraria thunbergiana, and irisolidone, a metabolite of Kakkalide produced by intestinal microflora, against carrageenan-induced inflammation in air pouches on the backs of mice and in lipopolysaccharide (LPS)-stimulated peritoneal macrophages were investigated. Kakkalide and irisolidone down-regulated the gene expression of cytokines [tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1β)] and cyclooxygenase-2 (COX-2) and the production of pro-inflammatory cytokines, TNF-α and IL-1β, and inflammatory mediators, NO and prostaglandin E(2) (PGE(2)), in LPS-stimulated peritoneal macrophages. These agents also inhibited the phosphorylation of IκB-α and the nuclear translocation of nuclear factor-kappa B (NF-κB). Orally administered Kakkalide and irisolidone significantly reduced carrageenan-induced inflammatory markers, leukocyte number, and protein amount in the exudates of the air pouch. These constituents also inhibited PGE(2) production and COX-2 inducible nitric oxide synthase, IL-1β, and TNF-α expression. These agents also inhibited NF-κB activation. The anti-inflammatory effects of irisolidone were more potent than those of Kakkalide. Based on these findings, Kakkalide and irisolidone may inhibit inflammatory reactions via NF-κB pathway, and irisolidone, a metabolite of Kakkalide, may more potently inhibit these inflammatory reactions.
Kakkalide and irisolidone: HMG-CoA reductase inhibitors isolated from the flower of Pueraria thunbergiana
Biol Pharm Bull 2007 Oct;30(10):1965-8.PMID:17917273DOI:10.1248/bpb.30.1965.
As part of our search for anti-arteriosclerosis agents from traditional Chinese medicines, the 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase (HCR)-inhibitory constituent, Kakkalide, was isolated from the flower of Pueraria thunbergiana (PT, family Leguminosae). The antihyperlipidemic effects of Kakkalide and its metabolite, irisolidone, which may be a bioactive form in vivo and potently inhibit the HCR activity, were investigated in vivo. Both the oral and interperitoneal administrations of Kakkalide and irisolidone, with the exception of intraperitoneally treated Kakkalide, potently lowered the serum levels of total cholesterol (TC) and triglyceride (TG) in Trition WR1339-induced hyperlipidemic mice. The oral administrations of Kakkalide and irisolidone in hyperlipidemic mice induced, by the long-term feeding of a high fat diet, also potently reduced the serum levels of TC and TG and epididymal fat pad weight. These findings suggest that PT can improve hyperlipidemia, and the hypolipidemic effect may be due to HMG-CoA reductase.
Estrogenic effect of main components Kakkalide and tectoridin of Puerariae Flos and their metabolites
Biol Pharm Bull 2006 Jun;29(6):1202-6.PMID:16755017DOI:10.1248/bpb.29.1202.
To understand the relationship between the metabolism and estrogenic activity of Kakkalide and tectoridin, main isoflavones in the flower of Pueraria thunbergiana (family Leguminosae), these isoflavones and their metabolites by human intestinal microflora as well as their estrogenic effects were investigated. All human fecal specimens metabolized Kakkalide and tectoridin. All isolated kakkalide-hydrolyzing intestinal bacteria also hydrolyzed Kakkalide and tectoridin to irisolidone and tectorigenin, respectively. When the estrogenic effects of Kakkalide and tectoridin were compared with those of their metabolites irisolidone and tectorigenin, the metabolites more potently increased proliferation of MCF-7 cells than Kakkalide and tectoridin. These metabolites also potently induced estrogen-response c-fos and pS2 mRNA expression. These results suggest that Kakkalide and tectoridin may be metabolized mainly to irisolidone and tectorigenin, respectively, by intestinal microflora in the intestines, and which may be subsequently absorbed into the blood where they can express their estrogenic effect.