奥拉西坦联合尼莫地平对2型糖尿病认知功能障碍患者的临床研究

Efficacy of oxiracetam combined with nimodipine in the treatment of cognitive impairment patients with type 2 diabetes

目的评价奥拉西坦联合尼莫地平治疗2型糖尿病认知功能障碍患者的临床疗效,并探讨其作用机制。方法 90例2型糖尿病认知功能障碍患者随机分为奥拉西坦组(A组)30例,口服奥拉西坦800 mg,每天3次;尼莫地平组(B组)30例,口服尼莫地平20 mg,每天3次;联合用药组(C组)30例,同时口服上述2种药物,剂量相同。3组患者均治疗12周,比较治疗前后的蒙特利尔认知评价量表(Mo CA)评分、日常生活能力(ADL)评分、血清神经元特异性烯醇化酶(NSE)和S-100β蛋白的表达水平及不良反应发生率。结果与治疗前比较,治疗12周后,3组患者Mo CA评分均显著升高(P<0.05),ADL评分均显著降低(P<0.05),C组的上述指标变化更为显著(P<0.01)。A、B组治疗后血清NSE、S-100β表达较治疗前显著下降(P<0.05),C组下降更加显著(P<0.01)。3组患者服药期间均无明显不良反应发生。结论奥拉西坦联合尼莫地平可能通过降低NSE和S-100β表达而对糖尿病认知功能障碍起保护作用,其疗效比单一用药好,且不增加药品不良反应发生率。

Objective To evaluate the clinical efficacy and safety of oxiracetam combined with nimodipine on cognitive impairment patients with type 2 diabetes and to investigate its mechanisms. Methods Ninety patients with cognitive impairment in type 2 diabetes were randomly divided into oxiracetam group（ A）（ n = 30） with oxiracetam 800 mg,tid,po; nimodipine group（ B）（ n = 30） with nimodipine 20 mg,tid,po; and combined group（ C）（ n = 30） with oxiracetam plus nimodipine of the same dose. After tweleve-week treatment,the Montreal cognitive assessment（ Mo CA） and activities of daily living（ ADL） scale were evaluated. Neuron-specific enolase（ NSE） and S-100β protein expressions in blood serum and drug adverse reactions were also evaluated. Results After tweleve-week treatment,Mo CA score was significantly increased（ P〈0. 05） and ADL scale was significantly reduced in all of the three groups（ P〈0. 05）,and the changes in the C group was much more obvious than other two groups（ P〈0. 01）. After treatment,NSE and S-100β protein expressions in blood serum of group A and B were obviously reduced compared with before treatment（ P〈0. 05）,while group C were more dramatically reduced compared with A and Bgroup（ P〈0. 01）. No obvious side effect was observed in the period of treatment in all the three groups.Conclusion Oxiracetam combined with nimodipine treatment was superior to either of the single regiment in the treatment of cognitive impairment in type 2 diabetes without increasing the risk of developing side effect by inhibiting NSE and S-100β expressions.