摘要
目的探讨急性脑梗死患者血糖水平、氧化应激损伤程度及其相互关系。方法选择148例急性脑梗死患者按入院次日空腹血糖水平分成血糖升高组54例,血糖正常组94例,分别测定外周血清8-异前列腺素F2α(8-iso prostaglandin F2α,8-iso-PGF2α)和总超氧化物歧化酶(total superoxide dismutase,T-SOD)活力,并进行比对和统计学分析。结果高血糖组血清8-iso-PGF2a高于正常血糖组,T-SOD低于正常血糖组,差异均有统计学意义(P<0.01)。血糖水平和8-iso-PGF2α呈正相关(r=0.676,P<0.01),血糖水平与T-SOD活力呈负相关(r=-0.708,P<0.01)。8-iso-PGF2α与T-SOD活力也呈负相关(r=-0.712,P<0.01)。结论高血糖可能加剧急性脑梗死患者神经系统损害,其可能通过促进氧化应激损伤增加,抗氧化能力降低,促进了急性脑梗死的发展。
Objective To exploring the relationship between levels of blood glucose and oxidative stress damage in acute cerebral infarction. Methods 148 patients with acute cerebral infarction were selected according to the hospital the next day of fasting blood glucose level into hyperglycemia group 54 cases, 94 cases of normal blood sugar, The peripheral serum 8-iso prostaglandin F2α were measured (8 -iso prostaglandin F2, 8 -iso -PGF2α) and total superoxide dismutase (total superoxide dismutase, T - SOD) activity, and carries on the analysis comparison and statistic. Results High blood glucose group ser- um 8 - iso - PGF2α was higher than normal blood glucose group, T - SOD lower than the normal blood glucose group, the differ- ences were statistically significant (P 〈 0.01 ). The blood glucose levels was positively correlated with 8 -ise -PGF2α (r = 0. 676, P 〈 0. 01 ), but the blood glucose levels was negatively correlated with T - SOD activity ( r = - 0. 708, P 〈 0. 01 ). 8 - iso PGF 2α and T - SOD vitality also was a negative correlation ( r = - 0. 712, P 〈0. 01 ). Conclusion Hyperglycemia may aggravate damages to nervous systems in CI patients, which may be increased by promoting oxidative stress, reduced antioxidant capacity, and promote the development of acute cerebral infarction.
出处
《实用心脑肺血管病杂志》
2013年第5期36-37,共2页
Practical Journal of Cardiac Cerebral Pneumal and Vascular Disease
关键词
脑梗死
血糖
地诺前列素
超氧化物歧化酶
Brain infarction
Blood glucose
Dinoprost
Superoxide dismutase