Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The 12/15-lipoxygenase (LO) cascade governs the generation of 12-hydroperoxy-eicosatetraenoic acid (HPETE) and 15-HPETE from arachidonic acid. The 5-LO pathway plays a fundamental role in the biosynthesis of leukotrienes, essential inflammatory lipid mediators. Cyclooxygenase (COX)-1 and -2 biosynthetic pathways are responsible for prostaglandin and thromboxane formation. Experimental investigations in animal models using 12/15-LO deficient mice, 12/15-LO or 15-LO transgenic mice, or pharmacological 15-LO inhibition have all demonstrated the essential role of 12/15-LO in atherogenesis. The underlying mechanisms are linked to low-density lipoprotein oxidation, pro-inflammatory Th1 cytokine production and enhanced monocyte-endothelial cell interaction. Human genetic studies as well as disruption of the 5-LO gene in mouse models of hyperlipidemia revealed that 5-LO and 5-LO-activating protein are associated with risks of human cardiovascular disease, and that this cascade plays an important role in aortic aneurysm pathogenesis through leukotriene-mediated inflammatory chemokine production. COX-1 plays an active role in atherogenesis via thromboxane A(2), while COX-2-derived prostaglandin (PGI(2)) protects against atherosclerosis in murine models. Recent data demonstrated that selective inhibition of COX-2 augments the risk of cardiovascular events in patients. Selective inhibition or blockade of selective components in these two enzymatic pathways through systemic drug delivery or medical device approaches (e.g., drug-eluting stents) may have therapeutic benefit against certain cardiovascular diseases.
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PMID:Lipoxygenase and prostaglandin G/H synthase cascades in cardiovascular disease. 2047 20

Even though the role of all-trans lycopene from tomato in controlling atherosclerosis was reported, but no report is available on the cis-isomer of lycopene obtained from an easily available source green algae Chlorella marina. So in this study, Sprague Dawley rats fed with high-cholesterol diet were given standard drug lovastatin; algal lycopene (AL) (cis/all-trans 40:60) and tomato all-trans lycopene (TL) and the following parameters were studied. Total cholesterol, low-density lipoprotein, triglycerides were decreased significantly and the high-density lipoprotein levels were increased on treatment with AL. The activities of antioxidant enzymes catalase, superoxide dismutase, glutathione peroxidase, and glutathione reductase were found to be increased, whereas thiobarbituric acid reactive substances levels were decreased in AL when compared to the drug and TL-treated rats. The activities of inflammatory marker enzymes like cyclooxygenase, 15-lipoxygenase in monocytes and myeloperoxidase, C-reactive protein and ceruloplasmin levels in serum were found to be decreased on treatment with AL. Histopathological studies revealed that lycopene from this alga could reduce fatty liver and aortic plaque when compared to the drug and TL. Algal lycopene showed very significant antioxidant and anti-inflammatory effect in high-cholesterol fed rats. Therefore, AL from C. marina would be recommended for the treatment of hyperlipidemia.
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PMID:Effect of lycopene from Chlorella marina on high cholesterol-induced oxidative damage and inflammation in rats. 2388 96