OK “Bubbles” and “NSnewf ” You Wanted Proof Here You Go

I'm NOT advocating by any means  Bee Propolis is a cure or alternative just an enhancement.

US National Library of Medicine National Institutes of Health 

Adv Clin Exp Med. 2015 Mar-Apr;24(2):203-12. doi: 10.17219/acem/31792.
The Ethanol Extract of Polish Propolis Exhibits Anti-Proliferative and/or Pro-Apoptotic Effect on HCT 116 Colon Cancer and Me45 Malignant Melanoma Cells In Vitro Conditions.
Kubina R1, Kabała-Dzik A1, Dziedzic A2, Bielec B1, Wojtyczka RD3, Bułdak RJ4, Wyszyńska M1, Stawiarska-Pięta B1, Szaflarska-Stojko E1.
Author information
1
Department of Pathology, Medical University of Silesia, Sosnowiec, Poland.
2
Department of Conservative Dentistry with Endodontics, Medical University of Silesia, Bytom, Poland.
3
Department of Microbiology and Virology, Medical University of Silesia, Sosnowiec, Poland.
4
Department of Physiology, Medical University of Silesia, Zabrze, Poland.
Abstract
BACKGROUND:
Propolis is a natural product widely consumed in folk medicine. Different biological activities, such as anticancer, antioxidant, anti-inflammatory, antibiotic and antifungal effects have been reported for propolis and its constituents.
OBJECTIVES:
An in vitro study focused on an evaluation of the biological activity of EEPP, including its anti-proliferative influence on selected neoplastic cells, considering qualitative-quantitative chemical characterization of Polish propolis.
MATERIAL AND METHODS:
Cytotoxicity was evaluated by means of the MTT and LDH assays. The apoptosis was determined using fluorescence microscopy with annexin V-FITC. Additional EEPP composition was analyzed by a High Performance Liquid Chromatography (HPLC) method. The antimicrobial activity was evaluated by minimal inhibitory concentrations (MIC) against Streptococcus aureus, Enetecoccus faecalis, Escherichia coli, Pseudomonas aeruginosa and Candida albicans.

.
RESULTS:
The total content of flavonoids per quercetin in the examined propolis extract amounted to 0.442±0.091 mg/mL. The flavonoid compounds identified in Polish propolis included flavones, flavonones, flavonolols, flavonols and phenolic acids. The multi-directional interactions among the various chemical compounds in propolis seem to be the essential biological activities when considering its anticancer effects. The results showed that in case of Me45 and HCT 116 cell lines, the ethanol extract of propolis could inhibit cell growth as well as cell size reduction. Regarding antimicrobial activity, EEPP showed MICs ranging from 0.39 to 6.25 mg/mL.
CONCLUSIONS:
Ethanol extract of propolis from Poland obtained in the study exhibits anti-proliferative activity in different carcinoma cells.
PMID:
25931350
[Indexed for MEDLINE]

J Agric Food Chem. 2016 Jul 13;64(27):5484-9. doi: 10.1021/acs.jafc.6b01785. Epub 2016 Jul 1.
Effect of Okinawa Propolis on PAK1 Activity, Caenorhabditis elegans Longevity, Melanogenesis, and Growth of Cancer Cells.
Taira N1, Nguyen BC1, Be Tu PT1, Tawata S2.
Author information
Abstract
Propolis from different areas has been reported to inhibit oncogenic/aging kinase PAK1, which is responsible for a variety of conditions, including cancer, longevity, and melanogenesis. Here, a crude extract of Okinawa propolis (OP) was tested against PAK1 activity, Caenorhabditis elegans (C. elegans) longevity, melanogenesis, and growth of cancer cells. We found that OP blocks PAK1 and exhibits anticancer activity in the A549 cell (human lung cancer cell) line with IC50 values of 6 μg/mL and 12 μg/mL, respectively. Most interestingly, OP (1 μg/mL) significantly reduces reproduction and prolongs the lifespan of C. elegans by activating the HSP-16.2 gene, as shown in the PAK1-deficient strain. Furthermore, OP inhibits melanogenesis in a melanoma cell line (B16F10) by downregulating intracellular tyrosinase activity with an IC50 of 30 μg/mL. Our results suggest that OP demonstrated a life span extending effect, C. elegans, anticancer, and antimelanogenic effects via PAK1 inactivation; therefore, this can be a potent natural medicinal supplement against PAK1-dependent diseases.
KEYWORDS:
Caenorhabditis elegans; Okinawa propolis; PAK1; cancer; longevity; melanogenesis
PMID:
27337169
DOI:
10.1021/acs.jafc.6b01785
[Indexed for MEDLINE]

J Nat Prod. 2013 Aug 23;76(8):1399-405. doi: 10.1021/np400129z. Epub 2013 Jul 22.
Caffeic acid phenethyl ester inhibits alpha-melanocyte stimulating hormone-induced melanin synthesis through suppressing transactivation activity of microphthalmia-associated transcription factor.
Lee JY1, Choi HJ, Chung TW, Kim CH, Jeong HS, Ha KT.
Author information
Abstract
Caffeic acid phenethyl ester (1), a natural compound found in various plants and propolis, is a well-known anti-inflammatory, immunomodulatory, and cytotoxic agent. The present study aimed to investigate the molecular events underlying the antimelanogenic activity of 1 in alpha-melanocyte stimulating hormone (α-MSH)-stimulated B16-F10 melanoma cells. In this investigation, 1 effectively reduced α-MSH-stimulated melanin synthesis by suppressing expression of melanogenic enzymes such as tyrosinase, tyrosinase-related protein-1 (TRP-1), and tyrosinase-related protein-2 (TRP-2), although this compound did not directly inhibit tyrosinase enzyme activity. On the other hand, the expression and nuclear translocation of microphthalmia-associated transcription factor (MITF) as a key transcription factor for tyrosinase expression regulating melanogenesis were not affected by treatment with 1. The upstream signaling pathways including cAMP response element-binding protein (CREB), glycogen synthase kinase-3β (GSK-3β), and Akt for activation and expression of MITF were also not influenced by 1. Interestingly, 1 inhibited transcriptional activity of a tyrosinase promoter by suppressing the interaction of MITF protein with an M-box containing a CATGTG motif on the tyrosinase promoter. Given the important role of MITF in melanogenesis, suppression of 1 on the function of MITF to transactivate tyrosinase promoter may present a novel therapeutic approach to treat hyperpigmentation disorders.
PMID:
23876066
DOI:
10.1021/np400129z
[Indexed for MEDLINE]
 

Oncol Lett. 2016 Dec;12(6):4813-4820. doi: 10.3892/ol.2016.5251. Epub 2016 Oct 13.
Chrysin induces cell apoptosis in human uveal melanoma cells via intrinsic apoptosis.
Xue C1, Chen Y2, Hu DN3, Iacob C4, Lu C5, Huang Z1.
Author information
Abstract
Uveal melanoma is the most common intraocular malignant tumor in adults. Chrysin is a flavonoid present in honey, propolis, various plants and herbs. In the present study, the cytotoxic effects of chrysin were investigated on human uveal melanoma cell lines (M17 and SP6.5) and associated signaling pathways, and a comparison to the effects on normal ocular cells [scleral fibroblasts and retinal pigment epithelial (RPE) cells] was performed. The effects of chrysin on cell viability were assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Cell apoptosis was determined by using terminal deoxynucleotidyl transferase mediated dUTP nick end-labeling assay. Mitochondrial permeability was determined by JC-1 fluorescein analysis. Cytosol cytochrome c levels, and the activities of caspase-3, -8 and -9 were measured by enzyme-linked immunosorbent assay or colorimetric assay. Chrysin reduced the viability of cultured human melanoma cells in a dose-dependent manner (0, 10, 30 and 100 µM) with IC50 at 28.3 and 35.8 µM in SP6.5 and M17 cell lines, respectively. Chrysin at 30-100 µM levels selectively reduced the viability of melanoma cells without affecting the viability of scleral fibroblasts and RPE cells. Chrysin increased mitochondrial permeability, the levels of cytosol cytochrome c, and caspase-9 and -3 activities, but not capase-8 activity in uveal melanoma cells. The results of the present study indicate that chrysin induces apoptosis of human uveal melanoma cells via the mitochondrial signaling pathway and suggest that chrysin may be a promising agent in the treatment of uveal melanoma.
KEYWORDS:
apoptosis; caspase-3; caspase-9; chrysin; cytochrome c; uveal melanoma
PMID:
28105189