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目的研究养血清脑颗粒对大鼠脑缺血再灌注损伤后脑组织中碱性成纤维细胞生长因子(b FGF)和血管内皮生长因子(VEGF)表达的影响。方法将SD大鼠随机分为假手术组、模型组和实验组,每组8只。模型组和实验组用线栓法制作大鼠大脑中动脉脑缺血再灌注模型。实验组于再灌注3 h后灌胃给予养血清脑颗粒1 g·kg~(-1),qd,连续给药7 d。假手术组和模型组于再灌注3 h后灌胃给予相同体积的灭菌0.9%Na Cl溶液。用免疫组织化学法和实时定量聚合酶链式反应法检测缺血区脑组织中b FGF和VEGF的表达。结果模型组、假手术组、实验组大鼠脑组织中b FGF阳性细胞数分别为(23.92±3.84),(3.78±0.58),(34.08±5.64);VEGF阳性细胞数分别为(26.87±4.56),(5.24±0.67),(37.45±6.29),模型组的b FGF和VEGF阳性细胞数与假手术组比较差异有统计学意义(P<0.05),实验组的b FGF和VEGF阳性细胞数与模型组比较差异有统计学意义(P<0.05)。结论养血清脑颗粒可通过促进b FGF和VEGF的表达,从而发挥对脑缺血再灌注损伤的神经保护作用。
Objective To study the effects of Yangxue Qingnao Granule on the expression of basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) after cerebral ischemia-reperfusion injury in rats. Methods SD rats were randomly divided into sham operation group, model group and experimental group, with 8 rats in each group. The middle cerebral artery occlusion (MCAO) cerebral ischemia-reperfusion model was made in the model group and the experimental group by thread occlusion. The experimental group was given Yangxue Qingnao granule 1 g · kg ~ (-1) by gavage 3 h after reperfusion, qd for 7 days. Sham-operation group and model group were administrated with the same volume of sterile 0.9% NaCl solution 3h after reperfusion. The expression of bFGF and VEGF in ischemic brain tissue was detected by immunohistochemistry and real-time quantitative polymerase chain reaction. Results The number of bFGF positive cells in model group, sham operation group and experimental group were (23.92 ± 3.84), (3.78 ± 0.58), (34.08 ± 5.64), respectively. The number of VEGF positive cells were (26.87 ± 4.56 ), (5.24 ± 0.67) and (37.45 ± 6.29) respectively. The number of bFGF and VEGF-positive cells in the model group was significantly different from that in the sham operation group (P <0.05). The number of bFGF and VEGF-positive cells in the experimental group Compared with the model group, the difference was statistically significant (P <0.05). Conclusion Yangxue Qingnao granule can play a neuroprotective role in cerebral ischemia-reperfusion injury by promoting the expression of b FGF and VEGF.