[P23] Copper Oxidized Human Low Density Lipoproteins (Oxidized LDL)20P-OX-L102
|Concentration:||1 mg / ml, determined by the Lowry method|
|Source:||From fresh human plasma that has tested negative for Hepatitis C, HIV-I and HIV-II antibodies as well as Hepatitis surface antigens.|
|Purification:||After series ultra centrifugations, Low Density Lipoprotein (LDL) is isolated from Human plasma (Density: 1.063) and then oxidized with Copper (Cu++).|
|Purity:||LDL purity ≥ 98 % by SDS-PAGE.|
|Buffer:||10 mM PBS, 140 mM NaCl, 0.5 mM EDTA, 0.02% NaN3, pH 7.0.|
|Storage:||2°C-8°C for Short and long-term storage. Centrifuge Before Use. DO NOT FREEZE!|
*The products are for research or manufacturing use only, not for use in human therapeutic or diagnostic applications.
There is a large body of evidence suggesting that oxidative modifications of low-density lipoproteins (LDL) contribute significantly to the initiation and/or progression of atherosclerosis. Circulating LDL particles are able to penetrate the endothelium of arterial walls and become oxidized, promote inflammation, and drive injury to the overlying endothelium and surrounding smooth muscle cells (Ross, 1999).
The oxidation of LDL in vitro is accelerated significantly by metal ions and is inhibited by chelating agents. Ox-LDL exhibited chemical and biological properties similar but not identical to cell-modified LDL (Steinbrecher et al. 1984). Many investigators studying oxidized LDL have used Cu2+-catalyzed oxidation as an experimental model (Gebicki et al. 1991). The Cu2+ oxidation model has been useful in exploring many facets of the LDL oxidation process and may have biological relevance.
Ross, R. “Atherosclerosis is an inflammatory disease.” American Heart J. 138 (1999): S419–S420.
Gebicki, J. M., Jurgens, G., and Esterbauer, H. (1991) in OxidatiVe Stress: Oxidants and Antioxidants (Sies, H., Ed.) pp 371-397, Academic Press, New York.
Steinbrecher, U. P., Parthasarathy, S., Leake, D. S., Witzum, J. L., and Steinberg, D. (1984) Proc. Natl. Acad. Sci. U.S.A. 81, 3883-3887.
|[P23]||2017||Yang, Tzu-Ching; Chang, Po-Yuan; Kuo, Tzu-Ling; Lu, Shao-Chun (2017): Electronegative L5-LDL induces the production of G-CSF and GM-CSF in human macrophages through LOX-1 involving NF-κB and ERK2 activation. In Atherosclerosis 267, pp. 1–9. DOI: 10.1016/j.atherosclerosis.2017.10.016.|
|[P23]||2017||Yang, Tzu-Ching; Chang, Po-Yuan; Lu, Shao-Chun (2017): L5-LDL from ST-elevation myocardial infarction patients induces IL-1β production via LOX-1 and NLRP3 inflammasome activation in macrophages. In American journal of physiology. Heart and circulatory physiology 312 (2), H265-H274. DOI: 10.1152/ajpheart.00509.2016.|
|[P23]||2014||Lee, Su Jin; Thien Quach, Cung Hoa; Jung, Kyung-Ho; Paik, Jin-Young; Lee, Jin Hee; Park, Jin Won; Lee, Kyung-Han (2014): Oxidized low-density lipoprotein stimulates macrophage 18F-FDG uptake via hypoxia-inducible factor-1α activation through Nox2-dependent reactive oxygen species generation. In Journal of nuclear medicine : official publication, Society of Nuclear Medicine 55 (10), pp. 1699–1705. DOI: 10.2967/jnumed.114.139428.|
|[P23]||2011||Kang, Jie; Xie, Chenghui; Li, Zhimin; Nagarajan, Shanmugam; Schauss, Alexander G.; Wu, Tong; Wu, Xianli (2011): Flavonoids from acai (Euterpe oleracea Mart.) pulp and their antioxidant and anti-inflammatory activities. In Food chemistry 128 (1), pp. 152–157. DOI: 10.1016/j.foodchem.2011.03.011.|