Sundaram V, Hanna A N, Lubow G P, Koneru L, Falko J M, Sharma H M
Department of Internal Medicine, College of Medicine, Ohio State University, Columbus 43210, USA.
Am J Med Sci. 1997 Nov;314(5):303-10. doi: 10.1097/00000441-199711000-00007.
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.
低密度脂蛋白（LDL）氧化是动脉粥样硬化发病机制的核心。我们之前已经表明，草药混合物玛赫西阿姆里特卡拉什 - 4（MAK - 4）和玛赫西阿姆里特卡拉什 - 5（MAK - 5）在体外可抑制铜离子（Cu +2）和内皮细胞诱导的LDL氧化，并且MAK - 4可减轻喂食这种草药混合物的渡边遗传性高脂血症兔的动脉粥样硬化。本研究评估MAK - 4和MAK - 5在体内的抗氧化活性。10名接受稳定降脂治疗的高脂血症患者接受MAK - 4和MAK - 5治疗18周。每6周进行一次血浆脂蛋白、血浆脂质过氧化物和LDL氧化研究。在基线和18周时测量载脂蛋白A、载脂蛋白B和脂蛋白（a）水平。在用MAK - 4和MAK - 5治疗12周后，观察到Cu +2和内皮细胞诱导的LDL氧化的滞后期呈时间依赖性增加，氧化传播期延迟。对于Cu(+2)催化的LDL氧化，MAK - 4和MAK - 5摄入基线时以及6周、12周和18周后的滞后期分别为6.66小时±0.19（平均值±平均标准误差）、6.77小时±0.31、7.22小时±0.24和18.00小时±0.73。对于内皮细胞诱导的LDL氧化，滞后期分别为14.89小时±0.77、13.33小时±0.50、20.22小时±0.76和20.00小时±0.79。血浆脂质过氧化物水平没有显著变化。血浆脂蛋白以及载脂蛋白A、载脂蛋白B和脂蛋白（a）水平未见显著变化。结果表明，MAK - 4和MAK - 5可抑制高脂血症患者的LDL氧化。因此，MAK - 4和MAK - 5可能对动脉粥样硬化的预防和治疗有用。
