Summary of Research Findings
Summary of Research Findings
Summary of Research Findings
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Antioxidant <strong>Research</strong> (continued)<br />
10. Title<br />
Inhibition <strong>of</strong> Low-Density Lipoprotein Oxidation by Oral Herbal Mixtures Maharishi Amrit Kalash-4 (MAK-4) and<br />
Maharishi Amrit Kalash-5 (MAK-5) in Hyperlipidemic Patients<br />
Publication<br />
The American Journal <strong>of</strong> the Medical Sciences, Vol. 314, No. 5, pp. 303-310, 1997.<br />
Authors<br />
Vidya Sundaram, M.D.,* Atef N. Hanna, Ph.D.,** Gary P. Lubow, M.D.,** Lata Koneru, M.D.,† James M. Falko,<br />
M.D.,* and Hari M. Sharma, M.D.**<br />
Conducted at<br />
*Department <strong>of</strong> Internal Medicine and **Department <strong>of</strong> Pathology, College <strong>of</strong> Medicine, The Ohio State<br />
University, Columbus, OH<br />
†Department <strong>of</strong> Internal Medicine, Riverside Methodist Hospital, Columbus, OH.<br />
<strong>Summary</strong><br />
Low-density lipoprotein (LDL) oxidation is central to the pathogenesis <strong>of</strong> atherosclerosis. This study evaluated<br />
the antioxidant activity <strong>of</strong> MAK-4 and MAK-5 in vivo. Ten hyperlipidemic patients prescribed stable hypolipidemic<br />
therapy were treated with MAK-4 and MAK-5 for 18 weeks. Plasma lipoprotein, plasma lipid peroxide,<br />
and LDL oxidation studies were performed every 6 weeks. Apolipoprotein A, apolipoprotein B, and lipoprotein<br />
(a) levels were measured at baseline and 18 weeks. After 12 weeks <strong>of</strong> treatment with MAK-4 and MAK-5, a timedependent<br />
increase in the lag phase and delay in the propagation phase <strong>of</strong> oxidation <strong>of</strong> LDL by Cu +2 and<br />
endothelial cells was seen. Lag phases at baseline and after 6, 12, and 18 weeks <strong>of</strong> MAK-4 and MAK-5 ingestion<br />
were 6.66 hours ± 0.19 (mean ± standard error <strong>of</strong> mean), 6.77 hours ± 0.31, 7.22 hours ± 0.24, and 18.00<br />
hours ± 0.73, respectively, for Cu +2 -catalyzed LDL oxidation. Lag phases were 14.89 hours ± 0.77, 13.33 hours<br />
± 0.50, 20.22 hours ± 0.76, and 20.00 hours ± 0.79, respectively, for endothelial cell-induced LDL oxidation.<br />
The levels <strong>of</strong> plasma lipid peroxide did not change significantly. No significant changes were seen in the plasma<br />
lipoproteins and the levels <strong>of</strong> apolipoprotein A, apolipoprotein B, and lipoprotein (a). The results show that<br />
MAK-4 and MAK-5 inhibit LDL oxidation in patients with hyperlipidemia. Therefore, MAK-4 and MAK-5 may be<br />
useful in the prevention and treatment <strong>of</strong> atheroslerosis.<br />
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