头孢曲松钠对大鼠脑缺血损伤的保护作用及其机制

Neuroprotective effect of ceftriaxone on focal cerebral ischemia in rats and its mechanism

目的探讨在大鼠局灶性脑缺血模型中应用头孢曲松钠对脑缺血损伤的保护作用及其相关机制。方法制备Wistar大鼠局灶性脑缺血模型，并按随机数字表法分为单纯缺血组（MCAO组）、头孢曲松钠治疗组（MCAO＋CTX组）和盐水对照组，其中MCAO＋CTX组为缺血90min时给予头孢曲松钠200mg／kg。缺血后24h、48h、7d时对各组大鼠进行神经行为学评分和脑水肿程度测定。同时比较各组大鼠皮层和海马谷氨酸转运体功能的差异。结果随着缺血时间延长，各组大鼠神经行为学评分逐渐提高；脑水肿在缺血后24h、48h时逐渐加重，至7d时已逐渐消退。与MCAO组比较，各时间点MCAO＋CTX组大鼠神经行为学评分明显提高，脑水肿程度明显减轻，伤侧皮层及海马谷氨酸转运体功能明显增强，差异均有统计学意义（P〈0．05）。结论头孢曲松钠对大鼠局灶性脑缺血损伤具有保护作用，其机制可能与增强谷氨酸转运体功能从而减轻谷氨酸神经毒性作用有关。

Objective To explore the neuroprotective effect of ceftriaxone on cerebral ischemia injury in rats with focal cerebral ischemia and its possible mechanism. Methods Focal cerebral ischemic models were established in Wistar rats and randomly divided into ischemic group （performed middle cerebral artery occlusion [MCAO]）, ceftriaxone （CTX） therapy group （given CTX at a dosage of 200 mg/kg 90 min after MCAO） and control group （given physiological saline only）. Twenty-four and 48 h, and 7 d after MCAO, neurological behaviors and cerebral edema level were evaluated in these 3 groups; glutamate transporter function in the cortex and hippocampus of rats was compared between each 2 groups. Results With time extended, neurological behaviors scores were obviously elevated in every group; and cerebral edema became worse at 24 and 48 h and decreased 7 d after MCAO. As compared with that in the ischemic group, glutamate transporter function, level of edema and neurological behaviors scores in cortex and hippocampus of rats in the CTX therapy group were statistically increased at different ischemic time points （P〈0.05）. Conclusion Ceffriaxone has a neuroprotective effect against focal cerebral ischemia in rats, which may relate to increased glutamate transporter function and reduced glutamate neurotoxicity.