輔酶Q10營養補充劑（300毫克/天）對肝癌病人氧化壓力、抗氧化酵素活性及發炎之影響

肝癌（hepatocellular carcinoma，HCC）高居臺灣致死癌症第二名。研究發現，HCC與較高的氧化壓力及發炎反應有關。輔酶Q10為內生性親脂溶性物質，許多臨床研究指出它是一個很好的抗氧化及抗發炎劑。本研究目的為給予肝癌病人輔酶Q10補充劑（300 mg/d）介入後對其氧化壓力及發炎反應之影響。本研究為ㄧ個單盲、隨機分派的介入性研究。我們招募經過病理診斷為HCC第一期或第二期肝癌病人（n = 42），後隨機分派至安慰劑組（n = 20）及輔酶Q10介入組（150 mg/b.i.d，300 mg/d，n = 22）。介入時間12週。研究期間測量受試者血漿輔酶Q10、維生素A與E、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、麩胱甘肽過氧化酶）及發炎指標（高敏感度C-反應蛋白、腫瘤壞死因子-α、介白素-6）濃度。結果發現，介入12週後，輔酶Q10補充劑顯著降低肝癌病人之丙二醛濃度（p = 0.04）及發炎指標濃度（高敏感度C-反應蛋白及介白素-6濃度，p < 0.01）；抗氧化酵素活性顯著較介入前高（超氧歧化酶、過氧化氫酶、麩胱甘肽過氧化酶，p < 0.01）。此外，受試者介入後輔酶Q10濃度與氧化壓力（丙二醛）呈顯著之負相關（r = -0.43，p = 0.01），與抗氧化酵素（超氧歧化酶，r = 0.31，p = 0.01、過氧化氫酶，r = 0.24，p < 0.05、麩胱甘肽過氧化酶，r = 0.25，p = 0.04）及維生素E濃度（r = 0.30，p = 0.01）呈顯著之正相關。因此，我們認為肝癌病人每日使用300毫克輔酶Q10補充劑，應可顯著提升其抗氧化能力及改善發炎反應。

Hepatocellular carcinoma (HCC) is the second cause of cancer death in Taiwan. A higher level of oxidative stress and inflammation play a key role in the progression of HCC has been reported. Many clinical studies have indicated that coenzyme Q10 is an endogenous lipid-soluble antioxidant and anti-inflammation agent. The purpose of this study was to examine the levels of oxidative stress and inflammation after coenzyme Q10 supplementation (300 mg/day) in patients with HCC. This study was designed as a single blinded, randomized, parallel, placebo-controlled study. Patients who were diagnosed with primary HCC by pathology (n = 42) were randomly assign to the placebo (n = 20) or the coenzyme Q10 [300 mg/day (Q10-300 group), n = 22] intervention groups. Intervention for 12 weeks. Plasma coenzyme Q10, vitamin A, vitamin E, oxidative stress (malondialdehyde, MDA), antioxidant enzymes [superoxidase dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx)], and inflammatory markers [high sensitivity C-reactive protein (hs-CRP), tumor necrosis factor- (TNF-), and interleukin-6 (IL-6)] were measured during the intervention. The levels of MDA (p = 0.04) and inflammatory markers (hs-CRP and IL-6, p < 0.01) were significantly decreased, and antioxidant enzymes activities were significantly increased (p < 0.01) after 12 weeks of coenzyme Q10 supplementation. In addition, coenzyme Q10 level was significantly negatively correlated with oxidative stress (MDA, r = -0.43, p = 0.01), and positively correlated with antioxidant enzymes activities (SOD, r = 0.31， p = 0.01; CAT, r = 0.24，p < 0.05; GPx, r = 0.25，p = 0.04) and the level of vitamin E (r = 0.30, p = 0.01). In conclusion, we suggest that coenzyme Q10 supplementation at a dose of 300mg/d may increase the antioxidation and decrease the inflammation in patients with HCC.