Genkwanin has antitumor, and anti-inflammatory activities, it enhances host immunity, decreases the inflammatory cytokine levels, and regulates the miR-101/MKP-1/MAPK pathway.Genkwanin may have anti-skin ageing activity, it can up-regulate the transcriptional activation of human type vii collagen gene promoter, stimulating the formation of anchoring fibrils at the basement membrane zone in skin contributed to preventing skin ageing; it also induces a decrease of melanin synthesis by inhibiting tyrosinase activity, it could as skin whitening agent in cosmetic preparations.
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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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PLoS One. 2014 May 6;9(5):e96741.
Genkwanin inhibits proinflammatory mediators mainly through the regulation of miR-101/MKP-1/MAPK pathway in LPS-activated macrophages.[Pubmed: 24800851
Genkwanin is one of the major non-glycosylated flavonoids in many herbs with anti-inflammatory activities. Although its anti-inflammatory activity in vivo has been reported, the potential molecular mechanisms remain obscure.
METHODS AND RESULTS:
In this study, by pharmacological and genetic approaches, we explore the anti-inflammatory effects of Genkwanin in LPS-activated RAW264.7 macrophages. Genkwanin potently decreases the proinflammatory mediators, such as iNOS, TNF-α, IL-1β and IL-6, at the transcriptional and translational levels without cytotoxicity, indicating the excellent anti-inflammatory potency of Genkwanin in vitro. Mechanism study shows that Genkwanin significantly suppresses the p38- and JNK-mediated AP-1 signaling pathway and increases the mitogen-activated protein kinase (MAPK) phosphatase 1 (MKP-1) expression at the posttranscriptional level. We also confirmed that microRNA-101 (miR-101) is a negative regulator of MKP-1 expression. Moreover, regardless of miR-101-deficient cells or miR-101-abundant cells, the suppression effects of Genkwanin on supernatant proinflammatory mediators' levels are far less than that in respective negative control cells, suggesting that Genkwanin exerts anti-inflammatory effect mainly through reducing miR-101 production. However, Genkwanin can't affect the level of phospho-Akt (p-Akt), indicating that the phosphorylation of Akt may be not responsible for the effect of Genkwanin on miR-101 production.
We conclude that Genkwanin exerts its anti-inflammatory effect mainly through the regulation of the miR-101/MKP-1/MAPK pathway.
Int. J.Cosmetic Sci., 2007, 29(4):332- 3.
Genkwanin up-regulates the transcriptional activation of human type vii collagen gene promoter.[Reference: WebLink
METHODS AND RESULTS:
In a recent study, stimulating the formation of anchoring fibrils at the basement membrane zone in skin contributed to preventing skin ageing, such as wrinkle formation. Expression of the type VII collagen gene induces the formation of anchoring fibrils composed mainly of collagen type VII. We therefore transiently transfected a keratinocyte cell line with the plasmids containing type VII collagen gene promoter located upstream of the luciferase gene.
We investigated the promoter activity under the presence of flavonoids and we found that Genkwanin up-regulates the transcriptional activation of human type VII collagen gene promoter.
Int Immunopharmacol. 2015 Dec;29(2):701-707.
Antitumor and immunomodulatory activity of genkwanin on colorectal cancer in the APC(Min/+) mice.[Pubmed: 26388189
Colorectal cancer is the third most common malignant tumor with high morbidity and mortality.
METHODS AND RESULTS:
To evaluate the antitumor effect of Genkwanin on colorectal cancer enhanced by western high-fat diet, we investigated the activity of Genkwanin on HT-29 and SW-480 human colorectal cancer lines in vitro and on the APC(Min/+) mice in vivo. In a cell culture system, six different inflammatory cytokines obviously stimulated two cancer cells growth in a concentration-dependent manner, while Genkwanin significantly inhibited HT-29 and SW-480 human colorectal cancer cells proliferation and inflammatory cytokine IL-8 secretion. In the APC(Min/+) mice, the body weights, spleen and thymus indexes and immunity cytokine secretions were significantly improved after oral administration 12.5 and 25mg/kg/day of Genkwanin. Besides, the tumor multiplicity changes and inflammatory cytokine levels were markedly reduced in two Genkwanin-treated groups. The dysplastic adenomatous changes were also obviously ameliorated in gut histopathology.
Taken together, our results indicated that Genkwanin had a better antitumor activity partly via enhancing host immunity and decreasing the inflammatory cytokine levels. Genkwanin may be an effective chemotherapeutic agent for the treatment of colorectal cancer.
Life Sci. 2016 Jan 1;144:80-5.
Effect of apigenin-7-glucoside, genkwanin and naringenin on tyrosinase activity and melanin synthesis in B16F10 melanoma cells.[Pubmed: 26656314
In this study, we have investigated the effects of apigenin-7-glucoside, Genkwanin and naringenin, on mouse melanoma B16F10 cell proliferation. Influence of these natural products on percentage cell distribution in cycle phases and melanogenesis was also studied.
METHODS AND RESULTS:
Cell viability was determined at various periods using the MTT assay, whereas effects of tested compounds on progression through the cell cycle were analyzed by flow cytometry. In addition, amounts of melanin and tyrosinase were measured spectrophotometrically at 475 nm. Besides, the mechanism involved on the death route induced by the tested molecules was evaluated using the bis-benzimide trihydrochloride coloration method (Hoechst 33258).
Apigenin-7-glucoside, Genkwanin and naringenin exhibited significant anti-proliferative activity against B16F10 melanoma cells after 24 and 48 h of incubation. Furthermore, apigenin-7-glucoside, Genkwanin and naringenin provoked an increase of subG0/G1, S and G2/M phase cell proportion with a significant decrease of cell proportion in G0/G1 phases. The results evaluated using Hoechst 33,258, confirm that the percentage of B16F10 cells observed in the sub G0/G1 phase were undergoing apoptosis. Moreover, apigenin-7-glucoside and naringenin revealed an ability to enhance melanogenesis synthesis and tyrosinase activity of B16F10 melanoma cells. Whereas Genkwanin induces a decrease of melanin synthesis by inhibiting tyrosinase activity.
Our results promote the introduction of Genkwanin in cosmetic preparations, as skin whitening agent, whereas apigenin-7-glucoside and naringenin should be introduced into cosmetic products as natural tanning agents.
Am J Chin Med. 2014;42(2):349-59.
Intestinal absorptive transport of Genkwanin from Flos genkwa using a single-pass intestinal perfusion rat model.[Pubmed: 24707867
METHODS AND RESULTS:
To investigate the absorptive transport behavior of Genkwanin and the beneficial effects of monoterpene enhancers with different functional groups, the single-pass intestinal perfusion (SPIP) of rats was used.
The results showed that Genkwanin was segmentally-dependent and the best absorptive site was the duodenum. The effective permeability coefficient (P eff ) was 1.97 × 10(-4) cm/s and the absorption rate constant (Ka) was 0.62 × 10(-2) s(-1). Transepithelial transportation descended with increasing concentrations of Genkwanin. This was a 1.4-fold increase in P eff by probenecid, whereas a 1.4-fold or 1.6-fold decrease was observed by verapamil and pantoprazole, respectively. Furthermore, among the absorption enhancers, the enhancement with carbonyl (camphor and menthone) was higher than that with hydroxyl (borneol and menthol).
The concentration-independent permeability and enhancement by coperfusion of probenecid indicated that Genkwanin was transported by both passive diffusion and multidrug resistance protein (MDR)-mediated efflux mechanisms.