Gossypetin
(Synonyms: 棉花素) 目录号 : GC38917
A flavonoid with diverse biological activities
Cas No.:489-35-0
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Gossypetin is a flavonoid that has been found in H. sabdariffa and has diverse biological activities.1,2,3 It inhibits the MAP2K kinases MKK3 and MKK6 in a concentration-dependent manner, as well as induces apoptosis and cell cycle arrest at the G2 phase in KYSE-450 and KYSE-510 esophageal cancer cells when used at a concentration of 20 ?M.1 Gossypetin scavenges DPPH radicals and inhibits copper-induced lipid peroxidation in cell-free assays.2 It reduces high-fat diet-induced increases in serum cholesterol, triglycerides, and LDL-cholesterol levels, as well as decreases aortic extracellular lipid and foam cell deposits in a rabbit model of atherosclerosis when administered at a dose of 10 mg/kg.3
1.Xie, X., Liu, K., Liu, F., et al.Gossypetin is a novel MKK3 and MKK6 inhibitor that suppresses esophageal cancer growth in vitro and in vivoCancer Lett.442126-136(2019) 2.Chen, J.-H., Tsai, C.-W., Wang, C.-P., et al.Anti-atherosclerotic potential of gossypetin via inhibiting LDL oxidation and foam cell formationToxicol. Appl. Pharmacol.272(2)313-324(2013) 3.Lin, H.-H.In vitro and in vivo atheroprotective effects of gossypetin against endothelial cell injury by induction of autophagyChem. Res. Toxicol.28(2)202-215(2015)
| Cas No. | 489-35-0 | SDF | |
| 别名 | 棉花素 | ||
| Canonical SMILES | O=C1C(O)=C(OC2=C1C(O)=CC(O)=C2O)C3=CC(O)=C(C=C3)O | ||
| 分子式 | C15H10O8 | 分子量 | 318.24 |
| 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 | 3.1423 mL | 15.7114 mL | 31.4228 mL |
| 5 mM | 0.6285 mL | 3.1423 mL | 6.2846 mL |
| 10 mM | 0.3142 mL | 1.5711 mL | 3.1423 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。
Gossypetin- based therapeutics for cognitive dysfunction in chronic unpredictable stress- exposed mice
Metab Brain Dis 2022 Jun;37(5):1527-1539.PMID:35377087DOI:10.1007/s11011-022-00971-0.
Chronic unpredictable stress (CUS) is a promising model for induction of cognition impairment. Stress induced memory dysfunction is linked to the activation of kynurenine (KYN) pathway. This pathway indicates that, chronic stress primarily promotes the release of excessive cortisol from the adrenal gland, which tends to activate microglia and further increases kynurenine and its downstream pathway, resulting in excessive quinolinic acid (QA), which further impairs brain derived neurotrophic factor (BDNF) levels and leads to neurodegeneration. Prior studies already established anti-oxidant and anti-depressant activity of Gossypetin. This research study was mainly conducted to elaborate neuroprotective activity of Gossypetin against CUS-induced cognition impairment via acting on kynurenine pathway. In this study, Swiss albino mice were exposed to various stressors for five weeks and then administered with Gossypetin (5, 10 and 20 mg/kg, i.p.) from the 4th to the 7th week (from day 22 to 49). Several behavioral tests were carried out between days 36 to 49 (6th and 7th week) and further corticosterone, neurotransmitters, oxidative stress, and brain-derived neurotrophic factor (BDNF) levels were measured. Results state that CUS exposed mice showed significant improvement in the behavioral pattern after Gossypetin treatment. Corticosterone levels and oxidative stress was also found to be significantly decreased in Gossypetin (10 and 20 mg/kg, i.p.) treated mice when compared with CUS exposed mice. Whereas, serotonin, norepinephrine and BDNF levels were also found to be increased after Gossypetin treatment. Hence, Gossypetin can be considered as a neuroprotective agent against cognition impairment caused by chronic unpredictable stress.
Gossypetin ameliorates 5xFAD spatial learning and memory through enhanced phagocytosis against Aβ
Alzheimers Res Ther 2022 Oct 21;14(1):158.PMID:36271414DOI:10.1186/s13195-022-01096-3.
Background: Microglia are the resident immune cells found in our brain. They have a critical role in brain maintenance. Microglia constantly scavenge various waste materials in the brain including damaged or apoptotic neurons and Aβ. Through phagocytosis of Aβ, microglia prevent the accumulation of Aβ plaque in the brain. However, in Alzheimer's disease (AD) patients, chronic exposure to Aβ makes microglia to become exhausted, which reduces their phagocytic activity against Aβ. Since microglia play an important role in Aβ clearance, enhancing microglial phagocytic activity against Aβ is a promising target for AD treatment. Therefore, there is a great need for therapeutic candidate that enhances microglial Aβ clearance while inhibiting microglia's pathogenic properties. Methods: In vivo studies were conducted with 5xFAD AD model mice by treating Gossypetin for 13 weeks through intragastric administration. Their spatial learning and memory were evaluated through behavior tests such as Y-maze and Morris Water Maze test. Hippocampus and cortex were acquired from the sacrificed mice, and they were used for histological and biochemical analysis. Also, mouse tissues were dissociated into single cells for single-cell RNA sequencing (scRNA-seq) analysis. Transcriptome of microglial population was analyzed. Mouse primary microglia and BV2 mouse microglial cell line were cultured and treated with fluorescent recombinant Aβ to evaluate whether their phagocytic activity is affected by Gossypetin. Results: Gossypetin treatment improved the spatial learning and memory of 5xFAD by decreasing Aβ deposition in the hippocampus and cortex of 5xFAD. Gossypetin induced transcriptomic modulations in various microglial subpopulations, including disease-associated microglia. Gossypetin enhanced phagocytic activity of microglia while decreasing their gliosis. Gossypetin also increased MHC II+ microglial population. Conclusions: Gossypetin showed protective effects against AD by enhancing microglial Aβ phagocytosis. Gossypetin appears to be a novel promising therapeutic candidate against AD.
Gossypetin is a novel MKK3 and MKK6 inhibitor that suppresses esophageal cancer growth in vitro and in vivo
Cancer Lett 2019 Feb 1;442:126-136.PMID:30391783DOI:10.1016/j.canlet.2018.10.016.
Gossypetin as a hexahydroxylated flavonoid found in many flowers and Hibiscus. It exerts various pharmacological activities, including antioxidant, antibacterial and anticancer activities. However, the anticancer capacity of Gossypetin has not been fully elucidated. In this study, Gossypetin was found to inhibit anchorage-dependent and -independent growth of esophageal cancer cells. To identify the molecular target(s) of Gossypetin, various signaling protein kinases were screened and results indicate that Gossypetin strongly attenuates the MKK3/6-p38 signaling pathway by directly inhibiting MKK3 and MKK6 protein kinase activity in vitro. Mechanistic investigations showed that arginine-61 in MKK6 is critical for binding with Gossypetin. Additionally, the inhibition of cell growth by Gossypetin is dependent on the expression of MKK3 and MKK6. Gossypetin caused G2 phase cell cycle arrest and induced intrinsic apoptosis by activating caspases 3 and 7 and increasing the expression of BAX and cytochrome c. Notably, Gossypetin suppressed patient-derived esophageal xenograft tumor growth in an in vivo mouse model. Our findings suggest that Gossypetin is an MKK3 and MKK6 inhibitor that could be useful for preventing or treating esophageal cancer.
Design of Gossypetin derivatives based on naturally occurring flavonoid in Hibiscus sabdariffa and the molecular docking as antibacterial agents
J Basic Clin Physiol Pharmacol 2021 Jun 25;32(4):707-714.PMID:34214320DOI:10.1515/jbcpp-2020-0455.
Objectives: This study was purposed to design Gossypetin derivatives which have higher activity than the parent compound found in Hibiscus sabdariffa and to find the most potent compound as the antibacterial agent. Methods: Twenty-five Gossypetin derivatives were designed by conjugation the molecular structure of Gossypetin with acyl group from some natural phenolic acids. The antibacterial activity was predicted by docking simulation on Escherischia coli DNA gyrase (PDB. 1KZN) which was performed by Molegro Virtual Docker. Potency as an antibacterial agent was evaluated based on binding affinity, hydrogen bond, and similarity of binding pattern with reference ligand Clorobiocin. Results: Almost all derivatives showed higher binding affinity than Gossypetin (docking score -113.43 kcal/mol). The most active compound was 3G19 with docking score -167.42 kcal/mol which was comparable to clorobiocin (docking score -167.75 kcal/mol). The compounds displaying higher activity than Gossypetin were belonged to 7,4'-dimethyl and 3,7,4'-trimethylgossypetin of coumaric acid, caffeic acid, and also ferulic acid. The compounds showed similar binding mode with clorobiocin especially in interaction with Asn46. Conclusions: Gossypetin derivatives designed by conjugating the Gossypetin with phenolic acyl increased in silico antibacterial activity of the parent compound. The 3,7,4'-trimethylgossypetin of coumaric acid was selected as the most potent compound for antibacterial agents.
Gossypetin Inhibits Solar-UV Induced Cutaneous Basal Cell Carcinoma Through Direct Inhibiting PBK/TOPK Protein Kinase
Anticancer Agents Med Chem 2019;19(8):1029-1036.PMID:30827262DOI:10.2174/1871520619666190301123131.
Background: Skin photoaging, skin inflammation and skin cancer are related with excessive exposure to solar UV. PDZ-binding kinase/T-LAK cell-originated protein kinase (PBK/TOPK), a member of the serine/threonine protein kinase, which regulates the signaling cascades of p38 mitogen-activated protein kinase (p38 MAPK) and extracellular signal regulated kinase 1/2 (ERK1/2). PBK/TOPK plays a significant role in solar-UV-induced cutaneous basal cell carcinoma (BCC), and targeting PBK/TOPK can be supposed to treat and prevent cutaneous BCC. Methods: The pathological feature and the expression level of PBK/TOPK in cutaneous BCC tissues of human were studied in clinical samples. SUV-induced the phosphorylation of p38 MAPK and ERK1/2 were demonstrated ex vivo. Moreover, the interaction between Gossypetin and PBK/TOPK were detected by in vitro kinase assay and Microscale thermophoresis (MST) assay. Furthermore, the effect of Gossypetin to solar UV-induced the activity of PBK/TOPK were detected ex vivo and in vivo. Results: The clinical samples showed that the expression levels of PBK/TOPK, phosphor-p38 MAPK and phosphor- ERK1/2 were up-regulated in cutaneous BCC tissues of human. The expression of phosphor-p38 MAPK or phosphor-ERK1/2 increased in a dose and time dependent manner after solar UV treatment in HaCaT cells. MTT cytotoxicity assay results showed that Gossypetin has no effect on HaCaT cells. In vitro kinase assay and MST assay results showed that Gossypetin bound with PBK/TOPK and suppressed PBK/TOPK activity. Ex vivo results showed Gossypetin inhibited solar UV-induced phosphorylation of PBK/TOPK, p38 MAPK, ERK1/2 and H2AX by suppressing PBK/TOPK activity. In vivo test results indicated that Gossypetin suppressed solar UV-induced increase of PBK/TOPK, phosphor-p38 MAPK, phosphor-ERK1/2 and phosphor- H2AX in SKH-1 hairless mice. Conclusion: Our data demonstrated that Gossypetin can alleviate solar-UV-induced cutaneous BCC by blocking PBK/TOPK, and Gossypetin could be a remarkable agent for treating solar-UV induced cutaneous basal cell carcinoma.