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周庆博,李鲁扬,贾青,郑广娟,毕建忠,邵念方.脑宁康颗粒对脑出血大鼠的脑保护作用[J].中国中西医结合杂志,2007,(9):814-818
脑宁康颗粒对脑出血大鼠的脑保护作用
Protective Effect of Naoningkang Granule on Brain in Intracerebral Hemorrhagic Rats
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DOI:
中文关键词:  脑出血  大鼠  凝血酶受体-1  细胞凋亡  脑水肿
英文关键词:intracerebral hemorrhage  rat  thrombin receptor-1  cell apoptosis  brain edema
基金项目:山东省自然基金项目(No.Y2002C26)
作者单位
周庆博 山东大学第二医院神经内科 
李鲁扬 山东大学齐鲁医院保健科 
贾青 山东医学科学院 
郑广娟 山东中医药大学细胞生物学实验室 
毕建忠 山东大学第二医院神经内科 
邵念方 山东中医药大学附属医院 
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中文摘要:
      目的研究依据清热解毒法制成的脑宁康颗粒对脑出血大鼠脑组织的保护作用及机制。方法将大鼠随机分为5组:假手术组、脑出血模型组、脑宁康小、中、大剂量组,采用胶原酶Ⅶ诱导大鼠脑出血模型,术后2h各治疗组给予不同剂量脑宁康颗粒灌胃,余组给予等容量生理盐水,连续用药3天和7天后取脑组织,采用HE染色观察脑组织病理形态学改变,免疫组织化学法和TUNEL法分别检测脑出血周围组织凝血酶受体-1(PAR-1)的表达和神经细胞凋亡情况,干湿比重法测定脑组织水肿情况。结果脑出血大鼠脑组织PAR-1表达增强,各脑宁康治疗组脑组织病理形态明显改善,脑组织PAR-1表达减少,TUNEL阳性细胞数减少,脑水肿减轻,与模型组比较差异有显著性(P<0.05,P<0.01)。结论脑出血后的脑组织PAR-1高表达可能介导了神经细胞凋亡和脑水肿,脑宁康颗粒对出血脑组织有保护作用,可能与其抑制脑出血后脑组织PAR-1表达、减少细胞凋亡,从而减轻脑水肿相关。
英文摘要:
      Objective To investigate the protective effect and mechanism of Naoningkang Granule (NG), a Chinese medicinal preparation formulated for clearing heat and detoxication, on brain tissue in intracerebral hemorrhagic (ICH) rats. Methods Rats were randomly divided into 5 groups: the sham operated group, the model group and the high-, medium-and low-dose NG groups. Collagenase Ⅶ was injected into caudate nucleus to induce rat model of ICH, corresponding dosage of NG was started to give to the 3 NG groups by gastrogavage 2 h after modeling, and saline of equal volume was given to the other 2 groups instead. The brain tissue of rats was taken in batches at the 3rd and 7th day for pathomorphological observation using HE stain, and detection of thrombin receptor-1 (PAR-1) expression and nerve cell apoptosis in the peripheral tissue of hemorrhagic brain with immunohistochemistry and TUNEL assay, as well as for measurement of water content in brain tissue by wet-to-dry weight method. Results PAR-1 expression elevated in the model rats. As compared with the model group, the pathomorphological changes significantly improved, PAR-1 expression decreased, apoptotic cells reduced and brain edema alleviated in the 3 NG groups. Conclusion Overexpression of PAR-1 in the brain tissue might mediate the nerve cell apoptosis and brain edema in ICH rats. The mechanism of NG in protecting hemorrhagic brain tissue might be related with its actions in inhibiting the post-cerebral high PAR-1 expression to reduce cell apoptosis and relieve brain edema.
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