亚硒酸钠对沙土鼠脑缺血/再灌注损伤的抗氧化作用

The protective effects of sodium selenite against cerebral ischemia/reperfusion (I/R) in gerbils

目的探讨亚硒酸钠对沙土鼠脑缺血/再灌注(I/R)损伤的保护作用及其机制。方法实验分3组。采用夹闭双侧颈动脉法制备沙土鼠前脑I/R(2,4 d)模型,焦油紫染色,光镜下观察各组海马CA1区神经元的形态变化,电镜下超微结构变化。同时测定脑组织中丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-PX)、超氧化物歧化酶(SOD)的含量。结果硒处理组沙土鼠脑I/R后,神经元病理损伤减轻,GSH-PX和SOD含量增多,与对照组比较有显著差异(P<0.01,P<0.05)。MDA含量减少。结论亚硒酸钠对沙土鼠脑I/R损伤具有保护作用,其机制可能和增强脑I/R早期脑组织中抗氧化酶的抗氧化作用有关,可能存在对脑缺血耐受的预处理机制。

Objective To study the protective effects and mechanisms of sodium selenite against cerebral ischemia/reperfusion （I/R） in gerbils. Methods 40 gerbils were randomly divided into three groups： sham-operated group,cerebral I/R group for 2days and 4days, cerebral I/R for 2days and 4days with sodium selenitetreated group. By clipping bilateral common carotid arteries after five minutes in bath cerebral I/R models were made. Contents of malondiadehyde （MDA）, glutathioneperoxidase （GSH-PX） and superoxidedismutase （SOD） in cerebral tissue were measured. The pathology of hippocampus was observed by light and electron microscope respectively. Results In the sodium selenite-treated I/R group the contents of GSH-PX and SOD was higher, compared to that in the I/R group （P〈0. 01, P〈0. 05 respectively）, while MI）A was lower. And the pathological findings showed lighter damage in selenium-treated group as compared with controls. Conlusions Sodium selenite could protect neurons against cerebral ischemia/reperfusion injury. The mechanisms may be related to enhancing the effect of antioxidant enzymes in cerebral tissue, inhibiting the damage of free radical and extenuating lipid peroxidation; preconditioning cerebral ischemia tolerance.