許多臨床研究指出冠狀動脈心臟病(coronary artery disease,CAD)與氧化壓力及慢性發炎有關。輔酶Q10為一種內生性親脂溶性抗氧化維生素,研究發現Statin類降血脂藥物可能會影響體內輔酶Q10的生合成。本研究目的為給予使用Statin類藥物之CAD受試者輔酶Q10補充劑(300毫克/天),觀察其對抗氧化及發炎變化之影響。CAD受試者從台中榮民總醫院心臟內科募集,經心導管檢查冠狀動脈狹窄程度大於或等於50 %,且服用Statin類降血脂藥物一個月以上者(n=51),隨機分派至安慰劑組(n=24)及輔酶Q10補充劑組(Q10-300組,n=27)。測量受試者血漿輔酶Q10、維生素A與E濃度、氧化壓力指標(丙二醛)、抗氧化酵素活性(超氧歧化酶、過氧化氫酶及麩胱甘肽過氧化酶)及發炎指標(高敏感C-反應性蛋白、腫瘤壞死因子 - α、介白素 - 6及脂締素)濃度。有42位受試者完成12週介入試驗(安慰劑組,n=19;Q10-300組,n=23)。結果顯示,介入12週後,Q10-300組之抗氧化酵素活性(p<0.05)及血漿維生素E(p=0.04)濃度顯著高於安慰劑組,而發炎指標(腫瘤壞死因子 - α及介白素 - 6)濃度顯著低於安慰劑組(p<0.05)。組內比較發現,Q10-300組介入12週後,可顯著提升抗氧化酵素活性(p<0.05)及降低發炎指標(腫瘤壞死因子 - α及介白素 - 6)濃度(p<0.05)。此外,血漿輔酶Q10濃度與抗氧化酵素活性及維生素E濃度呈顯著之正相關(p<0.05);與丙二醛、腫瘤壞死因子 - α及介白素 - 6濃度呈顯著之負相關(p=0.03)。因此,本研究推論CAD病人每天使用300毫克的輔酶Q10補充劑,可提升其抗氧化力及改善發炎反應。
A high oxidative stress and chronic inflammation may contribute to the pathogenesis of coronary artery disease (CAD). Coenzyme Q10 (CoQ10) is recognized as an endogenous lipid-soluble antioxidant. Recent studies indicate that Statin therapy may reduce the biosynthesis of CoQ10. The purpose of this study was to investigate the effects of a coenzyme Q10 supplement (300 mg/d) on antioxidation and inflammation in patients with CAD during Statin therapy. Patients who were identified by cardiac catheterization as having at least 50% stenosis of one major coronary artery and treated with Statin at least one month were enrolled in this study. The subjects (n=51) were randomly assigned to the placebo group (n=24) and CoQ10-supplement groups (Q10-300 group, n=27). The plasma concentrations of coenzyme Q10, vitamin A and E, oxidative stress marker (malondialdehyde, MDA) and antioxidant enzyme (superoxide dismutase, catalase, and glutathione peroxidase) activities, and inflammatory markers [high sensitivity C-reactive protein (hs-CRP), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and adiponectin (AD)] were measured. Forty-two subjects (placebo group, n=19; Q10-300 group, n=23) were completed 12 weeks intervention. The levels of antioxidant enzymes activities (p<0.05) and vitamin E (p=0.04) were significantly higher in the Q10-300 group, and the levels of inflammatory markers (TNF-α and IL-6) were significantly lower in the Q10-300 group than the placebo group at the 12th week. After 12 weeks supplementation, the levels of antioxidant enzyme activities (p<0.05) were significantly increased and the inflammatory markers (TNF-α and IL-6) (p<0.05) were significantly decreased in the Q10-300 group. The plasma CoQ10 concentration was significantly positive correlated with antioxidant enzymes activities and vitamin E (p<0.05), and negative correlated with MDA, TNF-α, and IL-6 (p=0.03). In conclusion, CoQ10 supplement at a dose of 300 mg/d may increase the antioxidation and decrease the inflammation in patients with CAD.