摘要
目的探索急性期脑梗死(ACI)合并2型糖尿病的氧化应激程度。方法入选急性脑梗死患者97例,其中合并2型糖尿病50例(ACI糖尿病组),无糖尿病者47例(ACI无糖尿病组)。观察入选ACI患者发病48 h的神经功能缺失程度评分(NIHSS)、改良Rankin评分(mRS)评分;检测空腹血糖、糖化血红蛋白、血脂、hs-CRP、炎性因子(IL-1、IL-6、TNF-α)和血清8-羟基脱氧鸟苷酸(8-OHdG)、丙二醛(MDA)和超氧化物歧化酶(SOD)水平。结果发病48 h ACI糖尿病组血清8-OHdG(0.73±0.38)ng·m L^(-1)和MDA(4.32±1.93)nmol·m L^(-1),较ACI无糖尿病组血清8-OHdG(0.51±0.31)ng·m L^(-1)和MDA(3.21±1.16)nmol·m L^(-1)均明显升高,差异有统计学意义(分别P=0.002和P=0.001)。SOD在两组中差异无统计学意义[(133.44±18.16)U·m L^(-1) vs(134.89±19.17)U·m L^(-1)]。IL-1、IL-6、TNF-α在ACI糖尿病组患者血清中均明显升高。结论 ACI糖尿病患者较无糖尿病患者存在更明显的氧化应激反应,针对这类患者进行清除自由基及减少氧化应激损伤可能对临床治疗有一定的指导意义。
Aim To explore the degree of oxidative stress in acute cerebral infarction (ACI) patients with type 2 diabetes mellitus (T2DM). Methods 97 Patients with ACI in our study, including 50 cases with T2DM (ACI with diabete), 47 cases without diabete (ACI without diabete). The scores of NIHSS and mRS were evaluated and the levels of blood glucose, HbAlc, blood lipid, hs-CRP, IL-1, IL-6, TNF-a, 8-OHdG, MDA, SOD were measured. Results 48 hours of onset of ACI, the levels of 8-OHdG in ACI patients with T2DM (0.73~0.38) ng'mL~ was significantly increased compared with ACI patients without T2DM (0.51+0.31) ng.mL-% (P=0.002). the levels of MDA in ACI patients with T2DM was also significantly higher than that in ACI patients without T2DM (4.32+1.93) nmol'mL-~ vs (3.21:L1.16) nmol'mL-~ (P=0.001). There were no significant differences in SOD in the two groups (133.44±18.16) U.mL^-1 and (134.89+19.17) U.mL^-1. Inflammatory factors (IL-1, IL-6, TNF-a) in patients with ACI complicated with type 2 diabetes were significantly increased than that in ACI patients without T2DM. Conclusion The ACI patients with T2DM have more pronounced oxidative stress reaction than those without diabetes. The inhibition of oxidative stress reaction should be suggested as a strategy in clinical treatment for this kind of patients.
出处
《中国临床神经科学》
2017年第1期54-60,共7页
Chinese Journal of Clinical Neurosciences
关键词
脑梗死
2型糖尿病
急性脑梗死
氧化应激
cerebral infarction
acute cerebral infatction
type 2 diabetes mellitus
oxidative stress