A randomized, double-blind clinical study of the effects of Ankascin 568 plus on blood lipid regulation

Sheng-Fu Liu, Yin-Ruei Wang, You-Cheng Shen, Chien-Li Chen, Chine-Ning Huang, Tzu-Ming Pan, Chin-Kun Wang, Sheng-Fu Liu, Yin-Ruei Wang, You-Cheng Shen, Chien-Li Chen, Chine-Ning Huang, Tzu-Ming Pan, Chin-Kun Wang

Abstract

Hyperlipidemia and inflammation play important roles in the development and progression of atherosclerosis. Atherosclerosis is regarded as an inflammatory response of blood vessels to injury at the start of atherosclerotic plaque formation, which then leads to cardiovascular events. Edible fungi of the Monascus species have been used as traditional Chinese medicines in East Asia for several centuries. The fermented products of Monascus purpureus NTU 568 possess a number of functional secondary metabolites including the anti-inflammatory pigments monascin and ankaflavin. Compounds derived from M. purpureus have been shown to have hypolipidemic effects. We aimed to evaluate the effects of M. purpureus NTU 568 fermentation product an extract (Ankascin 568 plus) containing monascin and ankaflavin on blood lipids in volunteers with borderline high levels of total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) by conducting a 12-week randomized, double-blind, placebo-controlled, adaptive-design study. This study enrolled 40 subjects aged 18-65 years from a population of patients with TC and LDL-C levels of ≥180 mg/dL and 130-190 mg/dL, respectively. Measured endpoints included lipid profile, liver, kidney and thyroid function, electrolyte balance, creatinine phosphokinase, and fasting blood glucose. After 4 weeks of treatment (500 mg Ankascin 568 plus/day), the changes in the lipid levels showed that the active products had a more favorable effect than the placebo. Compared to the baseline, statistically significant decreases of 11.9% and 19.0% were observed in TC and LDL-C levels, respectively (p < 0.05 for all pairs). This study demonstrated that subjects administered one 500 mg capsule of Ankascin 568 plus for more than 4 weeks exhibited a significant reduction in serum TC and LDL-C levels. Therefore, Ankascin 568 plus may be a potentially useful agent for the regulation of blood lipids and the treatment of coronary artery diseases.

Keywords: Ankaflavin; Ankascin 568 plus; Hyperlipidemia; Monascin; Monascus purpureus NTU 568.

Copyright © 2017. Published by Elsevier B.V.

Figures

Fig. 1
Fig. 1
CONSORT flow diagram of patients with hyperlipidemia.

References

    1. Steinberg HO, Bayazeed B, Hook G, Johnson A, Cronin J, Baron AD. Endothelial dysfunction is associated with cholesterol levels in the high normal range in humans. Circulation. 1997;96:3287–93.
    1. Tandra S, Vuppalanchi R. Use of statins in patients with liver disease. Curr Treat Options Cardiovasc Med. 2009;11:272–8.
    1. Shepherd J, Cobbe SM, Ford I, Isles CG, Lorimer AR, Macfarlane PW, et al. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. N Engl J Med. 1995;333:1301–7.
    1. Delbosc S, Cristol JP, Descomps B, Mimran A, Jover B. Simvastatin prevents angiotensin II-induced cardiac alteration and oxidative stress. Hypertension. 2002;40:142–7.
    1. Manoukian AA, Bhagavan NV, Hayashi T, Nestor TA, Rios C, Scottolini AG. Rhabdomyolysis secondary to lovastatin therapy. Clin Chem. 1990;36:2145–7.
    1. Nakahara K, Kuriyama M, Sonoda Y, Yoshidome H, Nakagawa H, Fujiyama J, et al. Myopathy induced by HMG-CoA reductase inhibitors in rabbits: a pathological, electrophysiological, and biochemical study. Toxicol Appl Pharmacol. 1998;152:99–106.
    1. Corpier CL, Jones PH, Suki WN, Lederer ED, Quinones MA, Schmidt SW, et al. Rhabdomyolysis and renal injury with lovastatin use. Report of two cases in cardiac transplant recipients. JAMA. 1998;260:239–41.
    1. Tokinaga K, Oeda T, Suzuki Y, Matsushima Y. HMG-CoA reductase inhibitors (statins) might cause high elevations of creatine phosphokinase (CK) in patients with unnoticed hypothyroidism. Endocr J. 2006;53:401–5.
    1. Chen CL, Pan TM. Red mold dioscorea: a potentially safe traditional function food for the treatment of hyperlipidemia. Food Chem. 2012;134:1074–80.
    1. Shi YC, Pan TM. Characterization of a multifunctional Monascus isolate NTU 568 with high azaphilone pigments production. Food Biotechnol. 2010;24:349–63.
    1. Hsu WH, Lu SS, Lee BH, Hsu YW, Pan TM. Monacolin K and monascin attenuated pancreas impairment and hyperglycemia in BALB/c mice induced by advanced glycation endproducts. Food Funct. 2013a;4:1742–50.
    1. Hsu WH, Chen TH, Lee BH, Hsu WY, Pan TM. Monascin and ankaflavin act as natural AMPK activators with PPARα agonist activity to down-regulate nonalcoholic steatohepatitis in high-fat diet-fed C57BL/6 mice. Food Chem Toxic. 2014;64:94–103.
    1. Hsu WH, Lee BH, Liao TH, Hsu YW, Pan TM. Monascus-fermented metabolite monascin suppresses inflammation via PPAR-γ regulation and JNK inactivation in THP-1 monocytes. Food Chem Toxicol. 2012;50:1178–86.
    1. Hsu WH, Liao TH, Lee BH, Hsu YW, Pan TM. Ankaflavin regulates adipocyte function and attenuates hyperglycemia caused by high-fat diet via PPAR-γ activation. J Funct Foods. 2013b;5:124–32.
    1. Lee BH, Hsu WH, Hsu YW, Pan TM. Dimerumic acid attenuates receptor for advanced glycation endproducts signal to inhibit inflammation and diabetes mediated by Nrf2 activation and promotes methylglyoxal metabolism into dlactic acid. Free Radic Biol Med. 2013;60:7–16.
    1. Lee CL, Hung YP, Hsu YW, Pan TM. Monascin and ankaflavin have more anti-atherosclerosis effect and less side effect involving increasing creatinine phosphokinase activity than monacolin K under the same dosages. J Agric Food Chem. 2013;61:143–50.
    1. Yan R, Lin G, Ko NL, Tam YK. Low oral bioavailability and pharmacokinetics of senkyunolide a, a major bioactive component in Rhizoma Chuanxiong, in the rat. Ther Drug Monit. 2007;29:49–56.
    1. Sauret JM, Marinides G, Wang GK. Rhabdomyolysis. Am Fam Physician. 2002;65:907–12.
    1. Giannoglou GD, Chatzizisis YS, Misirli G. The syndrome of rhabdomyolysis: pathophysiology and diagnosis. Eur J Intern Med. 2007;18:90–100.
    1. Bonventre J, Shah S, Walker P, Humphreys M. Rhabdomyolysis-induced acute renal failure. In: Jacobson, Striker, Klahr, editors. The principles and practice of nephrology. 2nd ed. St. Louis: Mosby; 1995. pp. 564–76.
    1. Moore KP, Holt SG, Patel RP, Svistunenko DA, Zackert W, Goodier D, et al. A causative role for redox cycling of myoglobin and its inhibition by alkalinization in the pathogenesis and treatment of rhabdomyolysis-induced renal failure. J Biol Chem. 1998;273:31731–7.
    1. Homsi E, Barreiro MF, Orlando JM, Higa E. Prophylaxis of acute renal failure in patients with rhabdomyolysis. Ren Fail. 1997;19:283–8.
    1. Wortmann RL, Tipping RW, Levine JG, Melin JM. Frequency of myopathy in patients receiving lovastatin. Am J Cardiol. 2005;95:983–5.
    1. Brown CV, Rhee P, Chan L, Evans K, Demetriades D, Velmahos GC. Preventing renal failure in patients with rhabdomyolysis: do bicarbonate and mannitol make a difference? J Trauma. 2004;56:1191–6.

Source: PubMed

スポンサーと協力者

医学的状態

薬物療法

3
購読する