Natural Taxifolin 90% To Inhibit Cancer Cell Superior Antioxidant Capacity

Product Description

Active Pharmaceutical Ingredient Taxifolin 90% To Inhibit Ovarian Cancer Cell

Taxifolin is non-mutagenic and low toxic compared to the related compound quercetin. It acts as a potential chemopreventive agent by regulating genes through an ARE-dependent mechanism. Taxifolin has been shown to inhibit ovarian cancer cell growth in a dose-dependent manner. There is also a strong correlation (with a correlation coefficient of 0.93) between the antiproliferative effects of dihydroquercetin (DHQ, taxifolin) derivatives in the skin of murine fibroblasts and human breast cancer cells.

The flavonoid Taxifolin, also known as Dihydroquercetin, has similar pharmacological effects to other flavonoids. Its antioxidant capacity, however, is superior to that of common flavonoids, and it is widely distributed and abundant, which is why its medicinal value is gradually becoming recognized. In practice, It is rarely used singly, but is often used in preparations such as silymarin along with silybin A, silybin B, isosilybin A, etc. With the exploration of its resources and medicinal potential goes deeper, the therapeutic efficacy and the medical value of taxifolin is becoming unambiguous. To help the future research, this article, after a review on pharmacological activities, focuses on the breakthroughs on the applications of taxifolin in treatment of diseases across human systems from 2019 to 2022, and look ahead the future therapeutic potentials of Taxifolin.

Dihydroquercetin is a kind of chemical substance extracted from larch, Douglas fir and other pine plants. It belongs to bioflavonoid vitamin P. It is easily soluble in ethanol, acetic acid and boiling water, and slightly soluble in cold water.It has the function of antioxidation and free radical scavenging.

As a flavonoid, Taxifolin has been found to have anti-inflammatory properties. It was found that Taxifolin inhibited the enhanced activity of NF-κB in cerebral ischemia-reperfusion injury rats and demonstrated that this is caused by taxifolin’s antioxidant action. Furthermore, Taxifolin inhibits the infiltration of white blood cells and the expression of COX-2 and iNOS in cerebral ischemia-reperfusion injury, as well as the expression of Mac-1 and ICAM-1. The role of Taxifolin in modulating the inflammatory response in endotoxemia was investigated using Raw 264.7 cells and mice challenged with lipopolyssacharide (LPS) endotoxin. According to the results, Taxifolin treatment significantly decreased the transcription of TNF-α, IFN-γ, IL-10 and TLR-4 in Raw 264.7 cells. Additionally, taxifolin induced AMPK/Nrf2/HO-1 signaling axis and enhanced Nrf2 expression and phosphorylation. As a result of pretreatment with taxifolin, mice were significantly less likely to die after being exposed to the bacterial endotoxins LPS for 10 days. In addition, It was investigated that the effects of taxifolin on human mast cells (HMC-1), rat basophilic leukemia (RBL)-2H3, and bmMSCs. Specifically, they found that taxifolin inhibited the degranulation of bone marrow-derived mast cells, the production of leukotriene C4 (LTC4) and interleukin-6 (IL-6), and the expression of cyclooxygenase-2 (COX-2). Taxifolin can also inhibit the activation of RBL-2H3 and HMC-1 cells through Akt/IKK/NF-κB and MAPKs/cPLA2 signaling pathways (Pan et al., 2019). The results of these studies suggest that taxifolin could be a potential drug candidate for the treatment of allergic and inflammatory conditions.

Function of Taxifolin

Various pharmacological properties of taxifolin especially, antioxidant, anticancer, antimicrobial, anti-Alzheimer, hepatoprotective and cardioprotective were found. The most important observation is taxifolin showed better activity in vitro studies. Surprisingly, taxifolin showed effective anticancer, hepatoprotective and cardioprotective activities through multiple mechanisms.
1. Dihydroquercetin is not mutagenic and low toxic compared to the related compound quercetin. It acts as a potential chemopreventive agent by regulating genes via an ARE-dependent mechanism.
2.Taxifolin inhibited the cellular melanogenesis as effectively as arbutin, one of the most widely used hypopigmenting agents in cosmetics.