PectaSol Modified Citrus Pectin Powder Super-Nutrient to Support Cellular & Immune Health, Joint Support - 454 Grams - Formulated by Dr. Isaac Eliaz of ecoNugenics

£9.9
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PectaSol Modified Citrus Pectin Powder Super-Nutrient to Support Cellular & Immune Health, Joint Support - 454 Grams - Formulated by Dr. Isaac Eliaz of ecoNugenics

PectaSol Modified Citrus Pectin Powder Super-Nutrient to Support Cellular & Immune Health, Joint Support - 454 Grams - Formulated by Dr. Isaac Eliaz of ecoNugenics

RRP: £99
Price: £9.9
£9.9 FREE Shipping

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Fang T, Liu DD, Ning HM, Dan Liu, Sun JY, Huang XJ, et al. Modified citrus pectin inhibited bladder tumor growth through downregulation of galectin-3. Acta Pharmacol Sin. 2018;39:1885–93. Menachem A, Bodner O, Pastor J, Raz A, Kloog Y. Inhibition of malignant thyroid carcinoma cell proliferation by Ras and galectin-3 inhibitors. Cell Death Discov. 2015;1:15047. MCP inhibited the survival of TAM in hypoxia by reducing glucose uptake via downregulation of GLUT-1 in vitro Regular citrus pectin supports digestive health, but the molecules are too large to enter the circulation -- meaning benefits are restricted to the GI tract alone. PectaSol-C® MCP solves this limitation with an advanced modification process that reduces the size and structure of the pectin. This allows PectaSol-C® to absorb into the circulation and deliver total-body benefits related to cellular health, immunity and more.*

Modified citrus pectin inhibits breast cancer development in Modified citrus pectin inhibits breast cancer development in

MCP -mediated Gal-3 inhibition in mice prevented the profibrotic and proinflammatory effects of cardiotrophin-1 Similar results were obtained by Cheng et al. (2011) who tested the anti-tumor activity of different polysaccharide fractions isolated from ginseng on colon cancer HT-29 cells. While fractions rich in HG stopped cell cycle in G2/M phase, fractions rich in HG and modified by heat treatment exerted a much higher anti-proliferative activity, which was accompanied by caspase-3 activation and apoptosis induction ( Cheng et al., 2011). Similarly, potato pectin, rich in HG, inhibited in vitro HT-29 cell proliferation and provoked a cell cycle arrest in G2/M phase. This inhibition was due to a decrease in cyclin B1 expression and in CDK-1 activity ( Cheng et al., 2013). It is important to note that Kang et al. (2006) also produced a citrus pectin-derived oligosaccharide, which was biologically active, by irradiation, i.e., without chemical treatment. Pectin irradiated with 20 kGy and then dialyzed (WT <10,000) inhibited cancer cell growth. Immunopotentiating Activity of Pectin Maxwell, E. G., Belsham, N. J., Waldron, K. W., and Morris, V. J. (2012). Pectin - an emerging new bioactive food polysaccharide. Trends Food Sci. Technol. 24, 64–73. doi: 10.1016/j.tifs.2011.11.002 Dong S, Hughes RC. Macrophage surface glycoproteins binding to galectin-3 (Mac-2-antigen). Glycoconj J. 1997;14:267–74.Micrometastasis that transforms into clinically relevant secondary tumors eventually comes to depend on the development of new blood vessels via angiogenesis, the fifth and final rate-limiting step in metastasis. Galectin-3 promotes angiogenesis by serving as a chemoattractant for endothelial cells and in

PectaSol-C Modified Citrus Pectin, 150 g, Econugenics

Platt, D., and Raz, A. (1992). Modulation of the lung colonization of B16-F1 melanoma cells by citrus pectin. J. Natl. Cancer Inst. 84, 438–442. doi: 10.1093/jnci/84.6.438 Ryu JM, Lee HJ, Jung YH, Lee KH, Kim DI, Kim JY, et al. Regulation of stem cell fate by ROS-mediated alteration of metabolism. Int J Stem Cells. 2015;8:24–35. Pienta, K. J., Naik, H., Akhtar, A., Yamazaki, K., Replogle, T. S., Lehr, J., et al. (1995). Inhibition of spontaneous metastasis in a rat prostate cancer model by oral administration of modified citrus pectin. J. Natl. Cancer Inst. 87, 348–353. doi: 10.1093/jnci/87.5.348 Furthermore, WZB117, an inhibitor of GLUT-1, was introduced to confirm the role of GLUT-1 in the inhibitory effect of MCP. Compared with treatment with WZB117 alone, the combination of MCP at different concentrations and WZB117 did not enhance the inhibition of glucose uptake (Fig. 1e) and the survival of TAM in hypoxia obviously (Fig. 1f). This suggested that MCP could inhibit glucose uptake via downregulation of GLUT-1 expression, which in turn inhibited the survival of TAM, especially in the hypoxic microenvironment. Despite no effect on body weight, adipose tissue weights or adiposity, MCP prevented adipose tissue fibrosis, inflammation and the increase in adipocyte differentiation markers in a model of diet-induced obesityModified L. acidophilus ATCC 4356 cell envelope improved the bioavailability and the anti-(colon) cancer effect of MCP Cytotoxicity analysis of PectaSol-C was performed by MTT assay, as were parallel studies with the former brand version of MCP called PectaSol. Apoptosis and inhibition of cell growth were investigated by Western blotting. Patel, M., Shah, T., and Amin, A. (2007). Therapeutic opportunities in colon-specific drug-delivery systems. Crit. Rev. Ther. Drug Carrier Syst. 24, 147–202. doi: 10.1615/CritRevTherDrugCarrierSyst.v24.i2.20



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