|Description:||1. Gossypetin has anti-mutagenic, anti-atherosclerotic, antioxidant, as well as cytoprotective and antimicrobial effects. |
2. Gossypetin inhibits bone resorption through down-regulating lysosomal cathepsin K activity and autophagy-related protein induction in actin ring-bearing osteoclasts.
3. Gossypetin ameliorates ionizing radiation-induced oxidative stress in mice liver, it shows radioprotective action against gamma (γ)-radiation-induced oxidative stress.
4. Gossypetin is an inducer of apoptotic and autophagic cell death in LNCaP cells, and provide a new mechanism for its anticancer activity.
|Targets:||PI3K | ATPase | MMP(e.g.TIMP) | NF-kB | Nrf2 | JNK|
|Source:||The herbs of Rhodiola rosea|
|Solvent:||Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, 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: email@example.com
|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||3.1423 mL||15.7114 mL||31.4228 mL||62.8457 mL||78.5571 mL|
|5 mM||0.6285 mL||3.1423 mL||6.2846 mL||12.5691 mL||15.7114 mL|
|10 mM||0.3142 mL||1.5711 mL||3.1423 mL||6.2846 mL||7.8557 mL|
|50 mM||0.0628 mL||0.3142 mL||0.6285 mL||1.2569 mL||1.5711 mL|
|100 mM||0.0314 mL||0.1571 mL||0.3142 mL||0.6285 mL||0.7856 mL|
Mol Carcinog. 2017 Dec;56(12):2578-2592.
|Anti-prostate cancer potential of gossypetin via inducing apoptotic and autophagic cell death.[Pubmed: 28671312 ]|
|Gossypetin (GTIN), a naturally occurring hexahydroxy flavone, has been shown to possess antimutagenic, antioxidant, antimicrobial, and antiatherosclerotic effects. Here, we investigated the mechanism(s) underlying the anticancer potential of GTIN. In this study, investigations were showed that GTIN preferentially induces programed cell death of prostate cancer (PCa) cells in vitro and in vivo. MTT data showed that GTIN exhibited the anti-proliferation effect on human PCa cells in a dose- and time-dependent manner. Among two kinds of PCa cells, androgen-dependent LNCaP cells were the most susceptible to GTIN. GTIN was evaluated for apoptotic and autophagic activities in LNCaP cells, but not in androgen-independent DU145 cells with mutant Atg5 and resistant to autophagy. Molecular data showed the apoptotic effect of GTIN at a high dose in PCa cells might be mediated via mitochondrial pathway. The lower dose of GTIN-induced autophagy enhances LNCaP cell death, and is dependent on class III PI3K and Atg5 pathway. Finally, GTIN was evidenced by its inhibition on the growth of LNCaP cells in xenograft tumor studies. As a result, our data presented the first evidence of GTIN as an inducer of apoptotic and autophagic cell death in LNCaP cells, and provide a new mechanism for its anticancer activity.|
Journal of Functional Foods, 2016, 24:390-402.
|Dietary compound gossypetin inhibits bone resorption through down-regulating lysosomal cathepsin K activity and autophagy-related protein induction in actin ring-bearing osteoclasts[Reference: WebLink]|
|Gossypetin, usually isolated from the flowers and the calyx of Hibiscus sabdariffa, possesses anti-microbial and anti-atherosclerotic effects. However, anti-osteoporotic effects of Gossypetin have not been elucidated. Gossypetin attenuated RANKL-induced multinucleated osteoclast formation with enhanced TRAP activity and blunted bone resorption active in osteoclasts. Gossypetin inhibited the actin ring formation and αvβ3 integrin induction for sealing zones. This compound suppressed the induction of CAII, V-ATPase, ClC-7 and Ae2, all required for secretion of proton and chloride ions into resorption lacunae. Furthermore, Gossypetin reduced lysosomal cathepsin K transcription and MMP-9 activity, blunting accumulation of lysosomes in osteoclasts displaying an actin ring. The presence of Gossypetin deterred the induction of Rab7, and Atg12–Atg5 conjugate and Atg7 involved in LC3 lipidation, all prerequisites to osteoclast ruffled border formation. These observations demonstrate for the first time that Gossypetin was effective in retarding ruffled border formation and acidification in a sealed microenvironment of osteoclast resorption lacunae.|
Free Radic Res. 2015 Oct;49(10):1173-86.
|Gossypetin ameliorates ionizing radiation-induced oxidative stress in mice liver--a molecular approach.[Pubmed: 25994373 ]|
|Radioprotective action of Gossypetin (GTIN) against gamma (γ)-radiation-induced oxidative stress in liver was explored in the present article. Our main aim was to evaluate the protective efficacy of GTIN against radiation-induced alteration of liver in murine system. To evaluate the effect of GTIN, it was orally administered to mice at a dose of 30 mg/kg body weight for three consecutive days prior to γ-radiation at a dose of 5 Gy. Radioprotective efficacy of GTIN were evaluated at physiological, cellular, and molecular level using biochemical analysis, comet assay, flow cytometry, histopathology, immunofluorescence, and immunoblotting techniques. Ionizing radiation was responsible for augmentation of hepatic oxidative stress in terms of lipid peroxidation and depletion of endogenous antioxidant enzymes. Immunoblotting and immunofluorescence studies showed that irradiation enhanced the nuclear translocation of nuclear factor kappa B (NF-κB) level, which leads to hepatic inflammation. To investigate further, we found that radiation induced the activation of stress-activated protein kinase/c-Jun NH2-terminal kinase (SAPK/JNK)-mediated apoptotic pathway and deactivation of the NF-E2-related factor 2 (Nrf2)-mediated redox signaling pathway, whereas GTIN pretreatment ameliorated these radiation-mediated effects. This is the novel report where GTIN rationally validated the molecular mechanism in terms of the modulation of cellular signaling system' instead of ' This is the novel report where GTIN is rationally validated in molecular terms to establish it as promising radioprotective agents. This might be fruitful especially for nuclear workers and defense personnel assuming the possibility of radiation exposure.|
Medicinal Chemistry,2016, 6(2).
|Protective Role of Gossypetin against Cyclophosphamide Toxicity in Human Lymphocyte Culture In vitro[Reference: WebLink]|
|Gossypetin is a flavonoid which has anti-mutagenic, anti-atherosclerotic, antioxidant, as well as cytoprotective and antimicrobial effects. The objective of this study was to investigate the cytoprotective role of Gossypetin (GP) against cyclophosphamide (CP) toxicity in the human lymphocyte culture. Cytotoxic, necrotic and apoptotic effects of CP (1mM), GP (25, 50 and 100 μM) and combination of them (CP+GP) were studied by using MTT assay and Flow cytometry analysis. It was detected that CP significantly decreased cell viability rate via arresting cell cycle and increasing apoptosis/necroptosis. However, GP treatment reduced negative effects of CP at different concentrations. The most effective concentration of GP against CP toxicity was 25 μM. This concentration GP increased live cell number and cell viability, in addition decreased necrotic and late apoptotic cell quantity which were treated with CP. These results suggest that GP could attenuate the cytotoxic effects of CP and protect the healthy cells when it is used during chemotherapy.|