School of Nutrition, Chung Shan Medical University, Taichung 40201, Taiwan.
Nutr J. 2013 Nov 6;12(1):142. doi: 10.1186/1475-2891-12-142.
High oxidative stress and chronic inflammation can contribute to the pathogenesis of coronary artery disease (CAD). Coenzyme Q10 is an endogenous lipid-soluble antioxidant. Statins therapy can reduce the biosynthesis of coenzyme Q10. The purpose of this study was to investigate the effects of a coenzyme Q10 supplement (300 mg/d; 150 mg/b.i.d) on antioxidation and anti-inflammation in patients who have CAD during statins therapy.
Patients who were identified by cardiac catheterization as having at least 50% stenosis of one major coronary artery and who were treated with statins for at least one month were enrolled in this study. The subjects (n = 51) were randomly assigned to the placebo (n = 24) and coenzyme Q10 groups (Q10-300 group, n = 27). The intervention was administered for 12 weeks. The concentrations of coenzyme Q10, vitamin E, antioxidant enzymes activities (superoxide dismutase, catalase, and glutathione peroxidase), and inflammatory markers [C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6)] were measured in the 42 subjects (placebo, n = 19; Q10-300, n = 23) who completed the study.
The levels of the plasma coenzyme Q10 (P < 0.001) and antioxidant enzymes activities (P < 0.05) were significantly higher after coenzyme Q10 supplementation. The levels of inflammatory markers (TNF-α, P = 0.039) were significantly lower after coenzyme Q10 supplementation. The subjects in the Q10-300 group had significantly higher vitamin E (P = 0.043) and the antioxidant enzymes activities (P < 0.05) than the placebo group at week 12. The level of plasma coenzyme Q10 was significantly positively correlated with vitamin E (P = 0.008) and antioxidant enzymes activities (P < 0.05) and was negatively correlated with TNF-α (P = 0.034) and IL-6 (P = 0.027) after coenzyme Q10 supplementation.
Coenzyme Q10 supplementation at 300 mg/d significantly enhances antioxidant enzymes activities and lowers inflammation in patients who have CAD during statins therapy.
ClinicalTrials.gov Identifier: NCT01424761.
高氧化应激和慢性炎症可能导致冠状动脉疾病（CAD）的发病机制。辅酶 Q10 是一种内源性脂溶性抗氧化剂。他汀类药物治疗可减少辅酶 Q10 的生物合成。本研究的目的是探讨辅酶 Q10 补充剂（300mg/d；150mg，每日两次）对接受他汀类药物治疗的 CAD 患者的抗氧化和抗炎作用。
通过心脏导管检查确定至少有一条主要冠状动脉狭窄 50%的患者，并接受他汀类药物治疗至少一个月的患者被纳入本研究。将受试者（n=51）随机分为安慰剂组（n=24）和辅酶 Q10 组（Q10-300 组，n=27）。干预措施持续 12 周。在完成研究的 42 名受试者（安慰剂组，n=19；Q10-300 组，n=23）中测量了辅酶 Q10、维生素 E、抗氧化酶活性（超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶）和炎症标志物[C 反应蛋白（CRP）、肿瘤坏死因子-α（TNF-α）和白细胞介素-6（IL-6）]的浓度。
辅酶 Q10 补充后，血浆辅酶 Q10 水平（P<0.001）和抗氧化酶活性（P<0.05）显著升高。辅酶 Q10 补充后，炎症标志物（TNF-α，P=0.039）水平显著降低。与安慰剂组相比，Q10-300 组的受试者在第 12 周时维生素 E（P=0.043）和抗氧化酶活性（P<0.05）显著升高。血浆辅酶 Q10 水平与维生素 E（P=0.008）和抗氧化酶活性（P<0.05）呈显著正相关，与 TNF-α（P=0.034）和 IL-6（P=0.027）呈显著负相关。
辅酶 Q10 补充剂 300mg/d 可显著增强接受他汀类药物治疗的 CAD 患者的抗氧化酶活性并降低炎症反应。
ClinicalTrials.gov 标识符：NCT01424761。
