丙酮酸钠在脑缺血-再灌注损伤中的神经保护作用

目的 探讨丙酮酸钠（SP）对脑缺血-再灌注（IR）损伤的影响。方法 雄性SD大鼠24只，体重200~250g，随机分为三组：假手术+生理盐水组（S组）、脑IR+生理盐水组（M组）、脑IR+丙酮酸钠组（P组）。S组行假手术处理，M组、P组建立大脑中动脉梗死（MCAO）模型，阻断血流2 h，分别于血流再灌注时经尾静脉注射生理盐水或丙酮酸钠600 mg/kg。血流再灌注后24 h，采用TTC法测定脑梗死体积，采用mNSS评分测定神经功能缺损评分，采用Western blot法测定cleaved caspase-3、Bax、cleaved PARP-1蛋白含量以及细胞核内AIF蛋白含量，微板法测定谷胱甘肽（GSH）、超氧化物歧化酶（SOD）以及丙二醛（MDA）水平。结果 与S组比较，M组和P组脑梗死体积明显增加，mNSS评分明显升高；M组cleaved caspase-3、Bax、cleaved PARP-1蛋白含量和AIF细胞核内蛋白含量明显升高，GSH与SOD水平明显降低，MDA水平明显升高（P＜0.05）。与M组比较，P组脑梗死体积明显减小，mNSS评分明显降低，cleaved caspase-3、Bax、cleaved PARP-1蛋白含量和AIF细胞核内蛋白含量明显降低，GSH与SOD水平明显升高，MDA水平明显降低（P＜0.05）。结论 丙酮酸钠能够减轻大鼠脑IR损伤，其神经保护作用可能与减少细胞凋亡以及抑制氧化应激水平相关。

Neuroprotective effect of sodium pyruvate in cerebral ischemia-reperfusion injury

Objective To investigate the effect of sodium pyruvate (SP) on cerebral ischemia-reperfusion (IR) injury. Methods Twenty-four male SD rats, weighing 200-250 g, were randomly divided into 3 groups: sham operation and normal saline group (group S), IR and normal saline group (group M), IR and sodium pyruvate group (group P). Sham surgical treatment was performed in group S, and MCAO model was established in group M and group P to block the blood flow for 2 h. Normal saline or 600 mg/kg sodium pyruvate were injected into the caudal vein during blood reperfusion in each group. The volume of cerebral infarction was determined by TTC and the score of neural functional defect was determined by mNSS in 24 h after reperfusion. Western blot was used to determine cleaved caspase-3, Bax, cleaved PARP-1 protein content and AIF protein content in the nucleus. Glutathione (GSH), superoxide dismutase (SOD) and malondialdehyde (MDA) were determined by microplate method. Results Compared with group S, the cerebral infarction volume and mNSS score in group M was significantly increased, the protein content of cleaved caspase-3, Bax, cleaved parp-1 and the nuclear protein content of AIF were significantly increased, the levels of GSH and SOD were significantly decreased, and the MDA level was significantly increased (P < 0.05). Compared with group M, the cerebral infarction volume and mNSS score in group P was significantly reduced, the protein content of cleaved caspase-3, Bax, cleaved parp-1 and the nuclear protein content of AIF were significantly decreased, the levels of GSH and SOD were significantly increased, and the MDA level was significantly decreased (P < 0.05). Conclusion Sodium pyruvate can reduce brain IR damage in rats and its neuroprotective effect may be related to the reduction of cell apoptosis and inhibition of oxidative stress.