Karanjin
(Synonyms: 水黄皮素) 目录号 : GC63934
Karanjin 是 Fordia cauliflora 中主要的活性呋喃黄酮醇成分。Karanjin 通过提高 AMPK 的方式诱导骨骼肌细胞 GLUT4 易位。Karanjin 可通过细胞周期阻滞诱导癌细胞死亡，促进细胞凋亡。
Cas No.:521-88-0
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
Karanjin is a major active furanoflavonol constituent of Fordia cauliflora. Karanjin induces GLUT4 translocation in skeletal muscle cells by increasing AMPK activity. Karanjin can induce cancer cell death through cell cycle arrest and enhance apoptosis[1][2].
[1]. Jaiswal N, et al.Karanjin from Pongamia pinnata induces GLUT4 translocation in skeletal muscle cells in a phosphatidylinositol-3-kinase-independent manner. Eur J Pharmacol. 2011 Nov 16;670(1):22-8.
[2]. Guo JR, et al. Effects of karanjin on cell cycle arrest and apoptosis in human A549, HepG2 and HL-60 cancercells. Biol Res. 2015 Jul 26;48:40.
| Cas No. | 521-88-0 | SDF | Download SDF |
| 别名 | 水黄皮素 | ||
| 分子式 | C18H12O4 | 分子量 | 292.29 |
| 溶解度 | DMSO : 25 mg/mL (85.53 mM; ultrasonic and warming and heat to 60°C) | 储存条件 | 4°C, away from moisture and 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 | 3.4213 mL | 17.1063 mL | 34.2126 mL |
| 5 mM | 0.6843 mL | 3.4213 mL | 6.8425 mL |
| 10 mM | 0.3421 mL | 1.7106 mL | 3.4213 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。
Karanjin
Phytochemistry 2021 Mar;183:112641.PMID:33421890DOI:10.1016/j.phytochem.2020.112641.
Karanjin [IUPAC: 3-methoxy-2-phenylfuro-(2,3-h-chrome-4-ol)], a bioactive furanoflavonoid and a potent biomolecule, was first isolated from Pongamia pinnata (L.). The crude extracts from root, leaf and seed having active constituent Karanjin is highly valued in both traditional and modern knowledge systems. This review highlights, critically assesses, and presents the probable biosynthetic pathways of Karanjin and its isolation methodologies with a view to actualizing its full potential. Karanjin exhibits multiple health benefits and applications, with evident anti-diabetic, anti-cancer, anti-inflammatory, anti-hyperglycemic, antioxidant, anti-colitis, anti-ulcer, and anti-Alzheimer properties. Consequently, the physiochemical properties and biological effects of Karanjin have been detailed and analyzed. The efficacy of Karanjin has been attenuated by toxicological studies that have proven Karanjin to be non-toxic at physiological conditions as substantiated by in vitro and in vivo studies. In addition, the multiple insect repellent/insecticidal properties of Karanjin and its availability as an acaricide/bio-insecticide have been reviewed. This review article underscores and endorses the immense potential for novel drug leads in various medicinal and industrial applications, suggesting a deeper insight into its metabolic fate, bioavailability, and cellular effects that await further investigations.
The cytotoxicity of Karanjin toward breast cancer cells is involved in the PI3K/Akt signaling pathway
Drug Dev Res 2022 Nov;83(7):1673-1682.PMID:36065628DOI:10.1002/ddr.21986.
Karanjin is a bioactive furanoflavonoid with various pharmacological activities including anticancer activities. However, the effect and the related mechanism of Karanjin in breast cancer (BC) have not been revealed. The potential targets of Karanjin and BC were predicted using SwissTargetPrediction and GeneCards databases, respectively. The overlapping targets between Karanjin and BC were identified using the Venn diagram. DAVID database was used for the Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment pathway analysis. Cell viability, proliferation, and apoptosis were examined by MTT (3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-tetrazolium bromide), EdU (5-ethynyl-2'-deoxyuridine) incorporation, and TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP digoxigenin nick-end labeling) assays, respectively. The protein levels were measured by western blot analysis. We screened out 28 overlapping targets between Karanjin and BC. KEGG analysis showed that the targets of Karanjin in BC were associated with the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway. Karanjin inhibited cell viability and impeded the proliferative ability of BC cells. Moreover, Karanjin treatment induced apoptosis in BC cells. Additionally, Karanjin treatment blocked the PI3K/Akt signaling pathway and activation of the PI3K/Akt pathway reversed the antitumor effect of Karanjin on BC cells. In conclusion, Karanjin exerted antitumor activity in BC cells by regulating the PI3K/Akt signaling pathway.
Effects of Karanjin on dimethylhydrazine induced colon carcinoma and aberrant crypt foci are facilitated by alteration of the p53/Bcl2/BAX pathway for apoptosis
Biotech Histochem 2021 Apr;96(3):202-212.PMID:32580584DOI:10.1080/10520295.2020.1781258.
We investigated the effects of Karanjin on dimethylhydrazine (DMH) induced colon cancer in rats. Male Wistar rats were injected with DMH followed by dextran sodium sulfate in drinking water for 7 days. Karanjin at doses of 50,100 and 200 mg/kg was administered orally for 18 weeks. Colon tissues were investigated using TUNEL analysis of apoptosis; histopathological assessment including number of aberrant crypt foci (ACF); immunohistochemical staining for Bcl-2-associated X protein (BAX), B-cell lymphoma 2 (Bcl2), p53 and proliferating cell nuclear antigen (PCNA); and antioxidant assay in vivo. We found that treatment with Karanjin inhibited formation of ACF in the colon mucosa and reduced colon lesions. Karanjin treatment also increased the antioxidants, catalase, glutathione and superoxide dismutase. Immunostaining showed that Karanjin treatment reduced BAX, p53 and PCNA levels and increased Bcl2 expression. The TUNEL assay revealed that Karanjin induced apoptosis in the colon mucosa. Our findings suggest that Karanjin can ameliorate colon carcinogenesis in rats by regulating BAX, Bcl2 and p53 pathways.
Effect of Karanjin on 2,4,6-trinitrobenzenesulfonic acid-induced colitis in Balb/c mice
Indian J Pharmacol 2017 Mar-Apr;49(2):161-167.PMID:28706329DOI:10.4103/ijp.IJP_234_15.
Objectives: The objective of this study is to evaluate the beneficial effect of Karanjin for the treatment of experimental colitis. Methods: Colitis was induced in the Balb/c mice by rectal administration of 2% solution of 2,4,6-trinitrobenzenesulfonic acid (TNBS) in 50% methanol. Karanjin (>98% pure) was administered in two different concentrations 100 and 200 mg/kg and sulfasalazine (100 mg/kg) as reference for 7 consecutive days to colitic mice. On the 8 day, mice were euthanized and degree of inflammation was assessed by macroscopic, microscopic, histology and biochemical estimation of myeloperoxidase (MPO), nitric oxide (NO), malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD), and reduced glutathione (GSH) level were measured. Results: Karanjin significantly and dose dependently ameliorate the macroscopic damage, histological changes such as cellular infiltration, tissue necrosis, mucosal and submucosal damage as compared to the TNBS control group. Karanjin reduces the activity of MPO, depressed MDA, and NO level and helps in restoring the level of CAT, SOD, and GSH to normal when compared to the TNBS colitis group. Conclusion: Result of the present study indicates that Karanjin has the potential to cure colitis induced by intracolonic administration of TNBS.
Global transcriptome analysis reveals partial estrogen-like effects of Karanjin in MCF-7 breast cancer cells
Gene 2022 Jul 1;830:146507.PMID:35447244DOI:10.1016/j.gene.2022.146507.
Karanjin, an abundantly occurring furanoflavonoid in edible and non-edible legumes, exerts diverse biological effects in vivo, and in vitro. Its potential as an anticancer agent is gaining traction following recent demonstrations of its anti-proliferative, cell cycle inhibitory, and pro-apoptotic effects. However, the genomic correlates of these activities are not known. In the present study we delineated the transcriptomic footprint of 10 μM Karanjin in MCF-7 breast cancer cells, using next generation sequencing technology (RNA-seq). We show that karanjin-modulated gene-expression repertoire is enriched in several hallmark gene sets, which include early estrogen-response, and G2/M checkpoint genes. Genes modulated by Karanjin overlapped with those modulated by 1 nM 17β-estradiol (E2), or 1 μM tamoxifen. The results suggest partial estrogen-like activity of Karanjin, thereby presenting a caveat to its anticancer potential. Further investigations into its mechanisms of action are warranted to ascertain the true potential of Karanjin in anticancer, or endocrine therapy.