|Description:||1. Kakkalide is a potent lactate dehydrogenase (LDH) inhibitor. |
2. Kakkalide attenuates ethanol-induced gastric injury in mice by inhibiting the infiltration of neutrophils.
3. Kakkalide can inhibit ROS-associated inflammation and ameliorated insulin-resistant endothelial dysfunction by beneficial effects on IRS-1 function.
4. Kakkalide has anti-inflammatory effects, it ameliorates carrageenan-induced inflammation in mice by inhibiting NF-κB pathway.
5. Kakkalide shows protective effects on ethanol-induced lethality and hepatic injury are dependent on its biotransformation by human intestinal microflora.
|Targets:||IL Receptor | NF-kB | ROS | Akt | PI3K | IkB | NO | PGE | COX | TNF-α | IKK|
|Source:||The roots of Pueraria lobata|
|Solvent:||DMSO, Pyridine, Methanol, Ethanol, etc.|
|Storage:||Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
Need more advice on solubility, usage and handling? Please email to: firstname.lastname@example.org
|After receiving:||The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||1.6821 mL||8.4104 mL||16.8209 mL||33.6417 mL||42.0521 mL|
|5 mM||0.3364 mL||1.6821 mL||3.3642 mL||6.7283 mL||8.4104 mL|
|10 mM||0.1682 mL||0.841 mL||1.6821 mL||3.3642 mL||4.2052 mL|
|50 mM||0.0336 mL||0.1682 mL||0.3364 mL||0.6728 mL||0.841 mL|
|100 mM||0.0168 mL||0.0841 mL||0.1682 mL||0.3364 mL||0.4205 mL|
J Chromatogr B Analyt Technol Biomed Life Sci. 2017 Mar 24;1048:111-120.
|Extraction and isolation of potential anti-stroke compounds from flowers of Pueraria lobata guided by in vitro PC12 cell model.[Pubmed: 28236683]|
|A simple and efficient method based on ultrafiltration liquid chromatography-mass spectrometry (UFLC-MS) was applied to rapidly screen and identify ligands for lactate dehydrogenase (LDH) from the flowers of Pueraria lobata, and the compounds were assessed for anti-stroke activity using a PC12 cell model. Seven major isoflavones, Kakkalide, 3'-hydroxy puerarin, puerarin, puerarin xyloside, tectoridin, tectorigenin, and ononin, were identified as potent LDH inhibitors. A continuous online method, which consisted of microwave-assisted extraction and countercurrent chromatography (MAE-CCC), was newly developed for scaled-up production of these compounds with high purity and efficiency. This novel approach, using UFLC-MS coupled with MAE-CCC and a PC12 cell model, provided a powerful tool for screening, extraction, and separation of LDH inhibitors from complex samples, and a useful platform for the large-scale production of functional food and nutraceutical ingredients.|
Mol Nutr Food Res. 2017 Feb;61(2).
|Irisolidone attenuates ethanol-induced gastric injury in mice by inhibiting the infiltration of neutrophils.[Pubmed: 27546737]|
|This study was designed to determine whether irisolidone and its glycoside Kakkalide, which are the major constituents of the flower of Pueraria lobata (Kudzu) can attenuate ethanol-induced gastritic injury in mice. METHODS AND RESULTS: Irisolidone and Kakkalide inhibited IL-8 secretion and NF-κB activation in lipopolysaccharide-stimulated KATO III cells. Therefore, we investigated their protective effects against ethanol-induced gastric injury in mice. Pretreatment with Kakkalide or irisolidone decreased the area of hemorrhagic ulcerative lesions caused by ethanol and suppressed stomach myeloperoxidase activity, CXCL4 secretion, and NF-κB activation. The ameliorating effect of irisolidone was more potent than that of Kakkalide. CONCLUSION: Irisolidone may attenuate ethanol-induced gastritis by inhibiting the infiltration of immune cells, particularly neutrophils, through the regulation of CXCL-4 or IL-8 secretion.|
J Diabetes. 2013 Mar;5(1):13-24.
|Kakkalide ameliorates endothelial insulin resistance by suppressing reactive oxygen species-associated inflammation.[Pubmed: 23190749 ]|
|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.|
Inflammation. 2011 Oct;34(5):344-51.
|Kakkalide and its metabolite irisolidone ameliorate carrageenan-induced inflammation in mice by inhibiting NF-κB pathway.[Pubmed: 20686830]|
|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.|
J Pharmacol Sci. 2003 Nov;93(3):331-6.
|Protective effects of kakkalide from Flos puerariae on ethanol-induced lethality and hepatic injury are dependent on its biotransformation by human intestinal microflora.[Pubmed: 14646251]|
|When Kakkalide, which was isolated from Flos Puerariae, was incubated with human fecal bacteria, Kakkalide was metabolized to irisolidone via kakkalidone. When Kakkalide (250 mg/kg) was orally administered to rats, irisolidone, but not Kakkalide, was detected in the blood. The mortality associated with ethanol treatment was slightly reduced when the mice were intraperitoneally treated with Kakkalide. Intraperitoneally administered Kakkalide and kakkalidone did not reduce alcohol toxicity. However, orally administered Kakkalide and intraperitoneally administered irisolidone significantly reduced the mortality. Orally administered Kakkalide and intraperitoneally injected irisolidone greatly reduced serum alanine aminotransferase and aspartate aminotransferase activities in ethanol-intoxified mice. Orally administered Kakkalide and intraperitoneally administered irisolidone significantly lowered the level of blood ethanol. The results indicate that Kakkalide is a prodrug of irisolidone in protecting against ethanol-induced lethality and hepatic injury.|