Unidad de Investigación Cardiovascular, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, Jalisco, México.
J Diabetes Complications. 2012 Jul-Aug;26(4):352-8. doi: 10.1016/j.jdiacomp.2012.04.004. Epub 2012 May 16.
Diabetic polyneuropathy aetiology is based on oxidative stress generation due to production of reactive oxygen species. Ubiquinone is reduced to ubiquinol and redistributed into lipoproteins, possibly to protect them from oxidation.
To evaluate the impact of oral ubiquinone in diabetic polyneuropathy, and the role of lipid peroxidation (LPO) and nerve growth factor (NGF-β).
We conducted a double-blind, placebo-controlled clinical trial, patients were randomized to ubiquinone (400 mg) or placebo daily for 12 weeks. Main outcomes were clinical scores, nerve conduction studies, LPO, NGF-β and safety.
Twenty four patients on experimental group and twenty five on control group met the inclusion criteria (mean age 56 years, 22% male and 78% female, mean evolution of type 2 diabetes mellitus 10.7 years). Significant improvement on experimental vs control group was found in neuropathy symptoms score (from 2.5 ± 0.7 to 1 ± 0.8, p<0.001), neuropathy impairment score (5.5 ± 4 to 3.1 ± 2.6, p<0.001), sural sensory nerve amplitude (13.0 ± 6.1 to 15.8 ± 5.1 μV, p=0.049), peroneal motor nerve conduction velocity (39.7 ± 5.0 to 47.8 ± 4.9 m/s, p=0.047), and ulnar motor nerve conduction velocity (48.8 ± 6.8 to 54.5 ± 6.1m/s, p=0.046). There was a significant reduction of LPO in subjects treated with ubiquinone vs placebo (16.7 ± 8.6 and 23.2 ± 15.8 nmol/mL, respectively) with p<0.05, and NGF-β did not change (control 66.5 ± 26.7 vs. experimental 66.8 ± 28.4 pg/mL, p=0.856). No drug-related adverse reactions were reported.
Twelve weeks treatment with ubiquinone improves clinical outcomes and nerve conduction parameters of diabetic polyneuropathy; furthermore, it reduces oxidative stress without significant adverse events.
糖尿病多发性神经病的病因是由于活性氧物质的产生导致氧化应激。泛醌被还原为泛醇，并重新分布到脂蛋白中，可能是为了保护它们免受氧化。
评估口服泛醌对糖尿病多发性神经病的影响，以及脂质过氧化（LPO）和神经生长因子（NGF-β）的作用。
我们进行了一项双盲、安慰剂对照的临床试验，患者被随机分配到泛醌（400mg）或安慰剂组，每天服用 12 周。主要结局是临床评分、神经传导研究、LPO、NGF-β和安全性。
24 例实验组和 25 例对照组患者符合纳入标准（平均年龄 56 岁，22%为男性，78%为女性，2 型糖尿病平均病程 10.7 年）。实验组与对照组相比，神经病变症状评分（从 2.5±0.7 降至 1±0.8，p<0.001）、神经病变损伤评分（从 5.5±4 降至 3.1±2.6，p<0.001）、腓肠感觉神经振幅（从 13.0±6.1 增至 15.8±5.1μV，p=0.049）、腓总运动神经传导速度（从 39.7±5.0 增至 47.8±4.9m/s，p=0.047）和尺神经运动神经传导速度（从 48.8±6.8 增至 54.5±6.1m/s，p=0.046）均显著改善。与安慰剂组相比，接受泛醌治疗的患者 LPO 显著降低（分别为 16.7±8.6 和 23.2±15.8nmol/mL，p<0.05），而 NGF-β 无变化（对照组 66.5±26.7 与实验组 66.8±28.4pg/mL，p=0.856）。未报告与药物相关的不良反应。
12 周的泛醌治疗可改善糖尿病多发性神经病的临床结局和神经传导参数；此外，它还能降低氧化应激，而无明显不良反应。
