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)

Low-density lipoprotein (LDL) oxidation is central to the pathogenesis of atherosclerosis. We have shown previously that the herbal mixtures Maharishi Amrit Kalash-4 (MAK-4) and Maharishi Amrit Kalash-5 (MAK-5) inhibit LDL oxidation induced by cupric ions (Cu+2) and endothelial cells in vitro and that MAK-4 reduces atherosclerosis in Watanabe heritable hyperlipidemic rabbits that were fed this herbal mixture. This study evaluates the antioxidant activity of MAK-4 and MAK-5 in vivo. Ten hyperlipidemic patients prescribed stable hypolipidemic therapy were treated with MAK-4 and MAK-5 for 18 weeks. Plasma lipoprotein, plasma lipid peroxide, and LDL oxidation studies were performed every 6 weeks. Apolipoprotein A, apolipoprotein B, and lipoprotein (a) levels were measured at baseline and 18 weeks. After 12 weeks of treatment with MAK-4 and MAK-5, a time-dependent increase in the lag phase and delay in the propagation phase of oxidation of LDL by Cu+2 and endothelial cells was seen. Lag phases at baseline and after 6, 12, and 18 weeks of MAK-4 and MAK-5 ingestion were 6.66 hours +/- 0.19 (mean +/- standard error of mean), 6.77 hours +/- 0.31, 7.22 hours +/- 0.24, and 18.00 hours +/- 0.73, respectively, for Cu(+2)-catalyzed LDL oxidation. Lag phases were 14.89 hours +/- 0.77, 13.33 hours +/- 0.50, 20.22 hours +/- 0.76, and 20.00 hours +/- 0.79, respectively, for endothelial cell-induced LDL oxidation. The levels of plasma lipid peroxide did not change significantly. No significant changes were seen in the plasma lipoproteins and the levels of apolipoprotein A, apolipoprotein B, and lipoprotein (a). The results show that MAK-4 and MAK-5 inhibit LDL oxidation in patients with hyperlipidemia. Therefore, MAK-4 and MAK-5 may be useful in the prevention and treatment of atherosclerosis.
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PMID:Inhibition of low-density lipoprotein oxidation by oral herbal mixtures Maharishi Amrit Kalash-4 and Maharishi Amrit Kalash-5 in hyperlipidemic patients. 936 32

Fifty-eight healthy progeny (mean age +/- SD 13.9 +/- 7.9 years) of 39 families with a positive history for cardiovascular diseases ([CVD] n = 44) or hyperlipidemia (n = 14) were included in the study and were compared with 30 age-matched control participants, with a negative family history, to evaluate lipid profile, ceruloplasmin (Cp), and lipid peroxidation product (malondialdehyde [MDA]) levels, as well as in vitro copper-induced Low-density lipoprotein (LDL) oxidizability. Mean serum levels of total cholesterol, LDL cholesterol (LDL-C), apolipoprotein B-100, and MDA of the participants were significantly higher than those of the controls. Lag time, an LDL resistance oxidation marker, was lower in the study group and negatively correlated with LDL-C (r = -.437, P < .05) and Cp (r = -.272, P < .05) serum levels. In conclusion, progeny with a positive family history for CVD or hyperlipidemia have an atherogenic lipid profile and increased LDL susceptibility to oxidation. High Cp levels seem to be related to lower resistance of LDL to oxidation.
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PMID:Lipid profile, low-density lipoprotein oxidation and ceruloplasmin in the progeny of families with a positive history of cardiovascular diseases and/or hyperlipidemia. 1964 44