Taxifolin exhibits important anti-tyrosinase activity, it also exhibits significant inhibitory activity against collagenase with an IC50 value of 193.3 μM.Taxifolin has anti-oxidant, anti-melanogenic, chemopreventive, anti-inflammatory, and cardioprotective effects. Taxifolin promotes osteoblast differentiation in MC3T3-E1 cells and also inhibit osteoclastogenesis in RAW264.7 cells, it also can enhance andrographolide-induced mitotic arrest and apoptosis in human prostate cancer cells via spindle assembly checkpoint activation.
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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.
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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.
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Cancer Prev Res (Phila). 2012 Sep;5(9):1103-14.
Taxifolin suppresses UV-induced skin carcinogenesis by targeting EGFR and PI3K.[Pubmed: 22805054
Skin cancer is one of the most commonly diagnosed cancers in the United States. Taxifolin reportedly exerts multiple biologic effects, but the molecular mechanisms and direct target(s) of Taxifolin in skin cancer chemoprevention are still unknown.
METHODS AND RESULTS:
In silico computer screening and kinase profiling results suggest that the EGF receptor (EGFR), phosphoinositide 3-kinase (PI3K), and Src are potential targets for Taxifolin. Pull-down assay results showed that EGFR, PI3K, and Src directly interacted with Taxifolin in vitro, whereas Taxifolin bound to EGFR and PI3K, but not to Src in cells. ATP competition and in vitro kinase assay data revealed that Taxifolin interacted with EGFR and PI3K at the ATP-binding pocket and inhibited their kinase activities. Western blot analysis showed that Taxifolin suppressed UVB-induced phosphorylation of EGFR and Akt, and subsequently suppressed their signaling pathways in JB6 P+ mouse skin epidermal cells. Expression levels and promoter activity of COX-2 and prostaglandin E(2) (PGE(2)) generation induced by UVB were also attenuated by Taxifolin. The effect of Taxifolin on UVB-induced signaling pathways and PGE(2) generation was reduced in EGFR knockout murine embryonic fibroblasts (MEF) compared with EGFR wild-type MEFs. Taxifolin also inhibited EGF-induced cell transformation. Importantly, topical treatment of Taxifolin to the dorsal skin significantly suppressed tumor incidence, volume, and multiplicity in a solar UV (SUV)-induced skin carcinogenesis mouse model. Further analysis showed that the Taxifolin-treated group had a substantial reduction in SUV-induced phosphorylation of EGFR and Akt in mouse skin.
These results suggest that Taxifolin exerts chemopreventive activity against UV-induced skin carcinogenesis by targeting EGFR and PI3K.
PLoS One. 2013;8(1):e54577.
Taxifolin enhances andrographolide-induced mitotic arrest and apoptosis in human prostate cancer cells via spindle assembly checkpoint activation.[Pubmed: 23382917
Andrographolide (Andro) suppresses proliferation and triggers apoptosis in many types of cancer cells. Taxifolin (Taxi) has been proposed to prevent cancer development similar to other dietary flavonoids.
METHODS AND RESULTS:
In the present study, the cytotoxic and apoptotic effects of the addition of Andro alone and Andro and Taxi together on human prostate carcinoma DU145 cells were assessed. Andro inhibited prostate cancer cell proliferation by mitotic arrest and activation of the intrinsic apoptotic pathway. Although the effect of Taxi alone on DU145 cell proliferation was not significant, the combined use of Taxi with Andro significantly potentiated the anti-proliferative effect of increased mitotic arrest and apoptosis by enhancing the cleavage of poly(ADP-ribose) polymerase, and caspases-7 and -9. Andro together with Taxi enhanced microtubule polymerization in vitro, and they induced the formation of twisted and elongated spindles in the cancer cells, thus leading to mitotic arrest. In addition, we showed that depletion of MAD2, a component in the spindle assembly checkpoint (SAC), alleviated the mitotic block induced by the two compounds, suggesting that they trigger mitotic arrest by SAC activation.
This study suggests that the anti-cancer activity of Andro can be significantly enhanced in combination with Taxi by disrupting microtubule dynamics and activating the SAC.
Food Chem Toxicol. 2014 Jan;63:221-32.
Taxifolin prevents diabetic cardiomyopathy in vivo and in vitro by inhibition of oxidative stress and cell apoptosis.[Pubmed: 24269735
Diabetic cardiomyopathy has been increasingly recognized as an important cause of heart failure in diabetic patients. Excessive oxidative stress has been suggested to play a critical role in the development of diabetic cardiomyopathy.
METHODS AND RESULTS:
The objective of this study was to investigate the potential protective effects and mechanisms of Taxifolin on cardiac function of streptozotocin-induced diabetic mice and on hyperglycemia-induced apoptosis of H9c2 cardiac myoblasts. In vivo study revealed that Taxifolin improved diastolic dysfunction, ameliorated myocardium structure abnormality, inhibited myocyte apoptosis and enhanced endogenous antioxidant enzymes activities. Interestingly, Taxifolin reduced angiotensin II level in myocardium, inhibited NADPH oxidase activity, and increased JAK/STAT3 activation. In vitro investigation demonstrated that Taxifolin inhibited 33 mM glucoseinduced H9c2 cells apoptosis by decreasing intracellular ROS level. It also inhibited caspase-3 and caspase-9 activation, restored mitochondrial membrane potential, and regulated the expression of proteins related to the intrinsic pathway of apoptosis, thus inhibiting the release of cytochrome c from mitochondria into the cytoplasm.
In conclusion, Taxifolin exerted cardioprotective effects against diabetic cardiomyopathy by inhibiting oxidative stress and cardiac myocyte apoptosis and might be a potential agent in the treatment of diabetic cardiomyopathy.
Phytother Res. 2008 Sep;22(9):1200-7.
Flavonoids, taxifolin and luteolin attenuate cellular melanogenesis despite increasing tyrosinase protein levels.[Pubmed: 18729255
Flavonoids are a group of polyphenolic compounds widely distributed in plants. Their potent bio-activities and relatively low toxicity have rendered them useful ingredients in functional cosmetics. The purpose of the present study was to examine their potential effects on cellular melanogenesis. When tested in murine melanoma B16F10 cells activated by alpha-melanocyte stimulating hormone (alpha-MSH), Taxifolin and luteolin inhibited the cellular melanogenesis as effectively as arbutin, one of the most widely used hypopigmenting agents in cosmetics. As opposed to their antimelanogenic effects, Taxifolin and luteolin rather increased the tyrosinase protein levels in the absence and presence of alpha-MSH. However, these flavonoids effectively inhibited tyrosinase-catalysed oxidation of l-dihydroxyphenylalanine in cell-free extracts and in living cells. Furthermore, they attenuated cell pigmentation induced by expression of exogenous human tyrosinase. Therefore, the antimelanogenic effects of Taxifolin and luteolin are attributed to their inhibitory effects on tyrosinase enzymatic activity, despite their effects on increasing tyrosinase protein levels.
J Biomed Sci. 2006 Jan;13(1):127-41.
Taxifolin ameliorates cerebral ischemia-reperfusion injury in rats through its anti-oxidative effect and modulation of NF-kappa B activation.[Pubmed: 16283433
Flavonoids are a group of polyphenolic compounds widely distributed in plants. Their potent bio-activities and relatively low toxicity have rendered them useful ingredients in functional cosmetics. The purpose of the present study was to examine their potential effects on cellular melanogenesis.
METHODS AND RESULTS:
When tested in murine melanoma B16F10 cells activated by alpha-melanocyte stimulating hormone (alpha-MSH), Taxifolin and luteolin inhibited the cellular melanogenesis as effectively as arbutin, one of the most widely used hypopigmenting agents in cosmetics. As opposed to their antimelanogenic effects, Taxifolin and luteolin rather increased the tyrosinase protein levels in the absence and presence of alpha-MSH. However, these flavonoids effectively inhibited tyrosinase-catalysed oxidation of l-dihydroxyphenylalanine in cell-free extracts and in living cells. Furthermore, they attenuated cell pigmentation induced by expression of exogenous human tyrosinase.
Therefore, the antimelanogenic effects of Taxifolin and luteolin are attributed to their inhibitory effects on tyrosinase enzymatic activity, despite their effects on increasing tyrosinase protein levels.
Biochem Pharmacol. 2013 Nov 15;86(10):1476-86.
Quercitrin and taxifolin stimulate osteoblast differentiation in MC3T3-E1 cells and inhibit osteoclastogenesis in RAW 264.7 cells.[Pubmed: 24060614
Flavonoids are natural antioxidants that positively influence bone metabolism.
METHODS AND RESULTS:
The present study screened among different flavonoids to identify biomolecules for potential use in bone regeneration. For this purpose, we used MC3T3-E1 and RAW264.7 cells to evaluate their effect on cell viability and cell differentiation. First, different doses of chrysin, diosmetin, galangin, quercitrin and Taxifolin were analyzed to determine the optimum concentration to induce osteoblast differentiation. After 48h of treatment, doses ≥100μM of diosmetin and galangin and also 500μM Taxifolin revealed a toxic effect on cells. The same effect was observed in cells treated with doses ≥100μM of chrysin after 14 days of treatment. However, the safe doses of quercitrin (200 and 500μM) and Taxifolin (100 and 200μM) induced bone sialoprotein and osteocalcin mRNA expression. Also higher osteocalcin secreted levels were determined in 100μM Taxifolin osteoblast treated samples when compared with the control ones. On the other hand, quercitrin and Taxifolin decreased Rankl gene expression in osteoblasts, suggesting an inhibition of osteoclast formation. Indeed, osteoclastogenesis suppression by quercitrin and Taxifolin treatment was observed in RAW264.7 cells.
Based on these findings, the present study demonstrates that quercitrin and Taxifolin promote osteoblast differentiation in MC3T3-E1 cells and also inhibit osteoclastogenesis in RAW264.7 cells, showing a positive effect of these flavonoids on bone metabolism.
J Lipid Res. 2000 Dec;41(12):1969-79.
Modulation of hepatic lipoprotein synthesis and secretion by taxifolin, a plant flavonoid.[Pubmed: 11108730
METHODS AND RESULTS:
Infarction in adult rat brain was induced by middle cerebral arterial occlusion (MCAO) followed by reperfusion to examine whether Taxifolin could reduce cerebral ischemic reperfusion (CI/R) injury. Taxifolin administration (0.1 and 1.0 microg/kg, i.v.) 60 min after MCAO ameliorated infarction (by 42%+/-7% and 62%+/-6%, respectively), which was accompanied by a dramatic reduction in malondialdehyde and nitrotyrosine adduct formation, two markers for oxidative tissue damage. Overproduction of reactive oxygen species (ROS) and nitric oxide (NO) via oxidative enzymes (e.g., COX-2 and iNOS) was responsible for this oxidative damage. Taxifolin inhibited leukocyte infiltration, and COX-2 and iNOS expressions in CI/R-injured brain. Taxifolin also prevented Mac-1 and ICAM-1 expression, two key counter-receptors involved in firm adhesion/transmigration of leukocytes to the endothelium, which partially accounted for the limited leukocyte infiltration. ROS, generated by leukocytes and microglial cells, activated nuclear factor-kappa B (NF-kappaB) that in turn signaled up-regulation of inflammatory proteins. NF-kappaB activity in CI/R was enhanced 2.5-fold over that of sham group and was inhibited by Taxifolin. Production of both ROS and NO by leukocytes and microglial cells was significantly antagonized by Taxifolin.
These data suggest that amelioration of CI/R injury by Taxifolin may be attributed to its anti-oxidative effect, which in turn modulates NF-kappaB activation that mediates CI/R injury.