目的:研究不同剂量脑心通对实验性脑梗死大鼠神经功能障碍、脑水肿及脑组织中炎性细胞因子NF-κB表达的影响。方法:实验于2004-03/11在河北医科大学神经内科实验室进行,取成年健康雄性SD大鼠150只,制备大脑中动脉梗死模型,造模手术完毕后,将大鼠随机分为5组,即脑心通大剂量(4g/kg)组、中剂量(2g/kg)组、小剂量(1g/kg)组、生理盐水和假手术组(假手术组为4k造模组),各组又分为6,24,48,72h,7d5个亚组,每亚组均为6只大鼠。脑心通各剂量组均为灌胃给药,生理盐水组给同体积的生理盐水,于相应时间点进行行为学评分后处死动物快速取脑,应用干-湿重法观察脑含水量变化、苏木精-伊红染色观察梗死周围炎性细胞浸润、免疫组织化学方法观察脑组织中NF-κB表达。结果:150只大鼠经补充进入结果分析。①造模后大鼠手术对侧肢体存在不同程度瘫痪,术后48和72h时神经功能缺损最为明显,7d时神经功能基本恢复正常。②除假手术组外,其余各组在脑梗死后6h局部可见少量散在炎性细胞浸润;梗死后48h,炎性细胞浸润明显增多;并持续到7d。③与假手术组相比,其他各组NF-κB阳性细胞表达在各时间段均增加,梗死后6h开始增多,48h达高峰。脑心通大剂量组术后24,48h脑组织中NF-κB阳性细胞[(13.8±2.49)个,(21.0±3.16)个],比脑心通中剂量组[(21.0±3.54)个,(29.2±3.11)个]、脑心通小剂量组[(21.0±3.99),(31.2±2.59)个]和生理盐水组减少[(21.4±3.97)个,(33.8±1.30)]个表达明显(P<0.05)]。④与假手术组相比,其他各组脑组织含水量在各时间段均增加。术后24,48h脑含水量脑心通大剂量组[(78.95±1.36)%,(79.44±1.01)%]与脑心通中剂量组[(79.03±0.87)%,(80.46±1.54)%],明显低于同期的脑心通小剂量组[(79.21±0.68)%,(82.02±1.76)%]和生理盐水组[(79.30±1.11)%,(82.68±0.91)%P<0.05]。结论:脑心通干预可改善脑梗死大鼠的神经功能抑制炎性细胞因子NF-κB的表达,减轻脑水肿,保护神经元,其功能改善程度与脑心通剂量成正相关。 Objective: To study the effects of different doses of Naoxintong on neurological dysfunction, brain edema and expression of NF-κB in brain tissue of experimental cerebral infarction rats. METHODS: The experiment was performed at the Laboratory of Neurology, Hebei Medical University from March to November 2004. 150 adult healthy male Sprague-Dawley rats were selected to prepare a middle cerebral artery infarction model. After the completion of the model operation, the rats were randomly divided into 5 groups. , namely, Naoxintong high-dose (4g/kg) group, middle-dose (2g/kg) group, small-dose (1g/kg) group, physiological saline, and sham operation group (4k model group for sham operation group). The group was divided into 6, 24, 48, 72h, 7d5 subgroups, and each subgroup was 6 rats. Each group of Naoxintong was intragastrically administered, and the saline group was given the same volume of physiological saline. After the behavioral score was performed at the corresponding time point, the animals were sacrificed and the brains were quickly removed. The changes of brain water content were observed by dry-wet weight method. Hematoxylin-eosin staining was used to observe the infiltration of inflammatory cells around the infarct, and immunohistochemistry was used to observe the expression of NF-κB in brain tissue. Results: 150 rats were recruited into the results analysis. 1 There were different degrees of paralysis in contralateral limbs after surgery. The neurological deficits were most obvious at 48 and 72 hours after operation. The neurological function returned to normal at 7 days. 2 In addition to the sham group, a small amount of diffuse inflammatory cell infiltration was observed locally at 6 h after cerebral infarction in all the other groups. At 48 h after infarction, inflammatory cell infiltration was significantly increased and continued until 7 days. 3 Compared with the sham-operated group, the expression of NF-κB positive cells in other groups increased at each time period, increased at 6 h after infarction, and peaked at 48 h. In the high-dose Naoxintong group, the number of NF-κB positive cells in brain tissue was (13.8±2.49), (21.0±3.16), and that of Naoxintong was (21.0±3.54). (29.2±3.11), Naoxintong low-dose group [(21.0±3.99), (31.2±2.59)] and saline group decreased [(21.4±3.97), (33.8±1.30)] (P<0.05)]. 4 Compared with sham group, the water content of brain tissue in other groups increased at each time period. At 24 and 48 hours after operation, the brain water volume in the high-dose Naoxintong group [(78.95±1.36)%, (79.44±1.01)%] and the Naoxintong middle-dose group [(79.03±0.87)%, (80.46±1.54)% ], significantly lower than the same period of Naoxintong small dose group [(79.21 ± 0.68)%, (82.02 ± 1.76)%] and saline group [(79.30 ± 1.11)%, (82.68 ± 0.91)% P <0.05] . Conclusion: Naoxintong intervention can improve the neurological function of rats with cerebral infarction by inhibiting the expression of inflammatory cytokines like NF-κB, reducing cerebral edema, and protecting neurons. The degree of functional improvement is positively correlated with the brain-heart rate.