醒脑静注射液对颅脑损伤大鼠认知功能的影响

The effect of Xingnaojing injection on cognitive function of rats with traumatic brain injury

目的:揭示醒脑静注射液对颅脑损伤大鼠认知功能的影响及相关机制。方法:108只大鼠随机分为假手术组、外伤组和治疗组,每组36只。假手术组和外伤组大鼠每日腹腔注射1mL0.9%氯化钠溶液,治疗组大鼠每日按5mL/kg剂量腹腔注射醒脑静注射液,连续7d。取每组6只大鼠,采用Morris水迷宫实验记录逃避潜伏期。依次在造模后12、24、48、72和168h,取每组6只大鼠断头处死,取外伤灶周边脑组织TUNEL法检测凋亡神经细胞,Westernblot检测procaspase-3蛋白表达,免疫组织化学染色法检测caspase-3蛋白表达。结果:外伤组大鼠脑组织凋亡神经细胞比例、procaspase-3和caspase-3蛋白表达量及大鼠逃避潜伏期均较假手术组显著升高(P<0.05),治疗组大鼠上述指标均较外伤组显著下降(P<0.05)。结论:醒脑静注射液可能通过抑制caspase-3蛋白介导的神经细胞凋亡改善颅脑损伤大鼠的认知功能。

Objective： To investigate the effect of Xingnaojing injection on cognitive function of rats with traumatic brain injury and its related mechanisms. Methods： A total of 108 rats were randomly divided as sham-operation group, trauma group and treatment group, with 36 rats in each group. Rats were given an intraperito-neal injection of 1 mL normal saline in the sham-operation group and trauma group, while rats in treatment group were administered intraperitoneally with 5 mL/kg Xingnaojing injection once a day for 7 days. Escape latency was recorded using Morris water maze for 6 rats in each group. At 12, 24, 48, 72 and 168 h respectively after the model was established, 6 rats in each group were decapitated. Brain tissues surrounding traumatic lesion were obtained. Apoptotic neuronal cells were determined using TUNEL staining. Protein expressions of procaspase-3 were investigated using Western blot. Caspase-3 protein expressions were detected using immunohistochemical staining technique. Results： Percentage of apoptotic neuronal cells and protein expressions of procaspase-3 and caspase-3 in the rat brain tissues as well as escape latency of rats were signifcantly higher in the trauma group than in the sham-operation group （P〈0.05）. The preceding variables in rats were signifcantly lower in the treat-ment group than in the trauma group （P〈0.05）. Conclusion： Xingnaojing injection may improve cognitive func-tion of rats with traumatic brain injury via inhibiting caspase-3 mediated neuronal cellular apoptosis.