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目的通过了解急性脑梗死(cerebral infarction,CI)患者血清尿酸(uric acid,UA)水平、氧化应激损伤程度及其相互联系,探讨血尿酸升高及氧化应激损伤在60岁以上老年人急性脑梗死发生中的作用。方法随机选择60例急性脑梗死患者(≥60岁)作为脑梗死组和30例健康人为对照组,测定外周血清UA、8-异前列腺素F2a(8-iso prostaglandin F2a,8-iso PGF2a)水平和总超氧化物歧化酶(total superoxide dis-mutase,T-SOD)活力。结果脑梗死组血清UA、8-iso PGF2a水平均高于对照组(P<0.01),而T-SOD明显低于对照组(P<0.01)。血清UA和8-iso PGF2a之间呈正相关(r=0.698,P<0.01),UA和T-SOD活力呈负相关(r=-0.712,P<0.01)。8-iso PGF2a与T-SOD活力也呈负相关(r=-0.723,P<0.01)。脑梗死组高尿酸血症与正常血尿酸者相比,血浆8-iso PGF2a水平明显增高、T-SOD活力明显降低(P<0.01)。结论血清UA水平升高可能是CI的一个危险因素,其可能通过促进氧化应激损伤增加,抗氧化能力降低,导致了CI的发生发展。
Objective To investigate the relationship between serum uric acid (UA), the degree of oxidative stress injury and their relationship in patients with acute cerebral infarction (CI), and to explore the relationship between serum UA level and oxidative stress injury in the elderly over 60 years old The role of cerebral infarction. Methods Sixty patients with acute cerebral infarction (≥60 years old) were randomly selected as cerebral infarction group and 30 healthy volunteers as control group. The levels of UA, 8-iso prostaglandin F2a (8-iso PGF2a) And total superoxide dis-mutase (T-SOD) activity. Results The levels of serum UA and 8-iso PGF2a in cerebral infarction group were significantly higher than those in control group (P <0.01), while the levels of T-SOD in cerebral infarction group were significantly lower than those in control group (P <0.01). There was a positive correlation between serum UA and 8-iso PGF2a (r = 0.698, P <0.01), but negative correlation between UA and T-SOD (r = -0.712, P <0.01). There was also a negative correlation between 8-iso PGF2a and T-SOD (r = -0.723, P <0.01). Plasma hyperuricemia in patients with cerebral infarction compared with normal blood uric acid, plasma 8-iso PGF2a levels were significantly increased, T-SOD activity was significantly reduced (P <0.01). Conclusion Serum UA levels may be a risk factor for CI, which may lead to the occurrence and development of CI by promoting the increase of oxidative stress injury and decreasing the anti-oxidative capacity.