《中国康复理论与实践》 ›› 2015, Vol. 21 ›› Issue (11): 1245-1250.

• 国际会议报道 • 上一篇    下一篇

养血清脑颗粒对血管性痴呆大鼠海马CA1区超微结构及p38丝裂原活化蛋白激酶蛋白表达的影响

伞云琨,张晋霞,刘斌,刘颖,李世英
  

  1. 作者单位:华北理工大学附属医院神经内一科,河北唐山市 063000。
  • 收稿日期:1900-01-01 修回日期:1900-01-01 出版日期:2015-11-25 发布日期:2015-11-25

Effect of Yangxue Qingnao Granule on Ultrastructures and Expression of p38 Mitogen Activated Protein Kinases in CA1 Area of Hippocampus of Vascular Dementia Rats

SAN Yun-kun, ZHANG Jin-xia, LIU Bin, LIU Ying, LI Shi-ying
  

  1. First Department of Neurology, the Affiliated Hospital of North China University of Science and Technology, Tangshan, Hebei 063000, China
  • Received:1900-01-01 Revised:1900-01-01 Published:2015-11-25 Online:2015-11-25

摘要: 目的 观察养血清脑颗粒对血管性痴呆大鼠海马CA1区超微结构及p38丝裂原活化蛋白激酶(p38MAPK)蛋白表达的影响。方法 180只 Sprague-Dawley大鼠随机分为假手术组、血管性痴呆模型组(模型组)和养血清脑颗粒治疗组(治疗组),采用改良的Pulsinelli四血管阻断法制作血管性痴呆模型,分别在术后1、2、4、8周采用透射电镜观察大鼠海马CA1区超微结构变化,免疫组化法和 Western blotting法检测海马 CA1区 p38MAPK水平。结果 模型组海马 CA1区神经元大量固缩,细胞核溶解,异染色质边集,线粒体肿胀。治疗组海马CA1区神经元核膜较完整,核染色质分布较均匀,胞质内线粒体及其他细胞器基本正常。与假手术组相比,模型组各时间点p38MAPK蛋白表达明显增多(P<0.01),4周时达高峰;与模型组比较,治疗组各时间点p38MAPK蛋白表达明显减少(P<0.01)。结论 养血清脑颗粒可改善血管性痴呆模型大鼠海马 CA1 区损伤的神经元超微结构,可能与抑制p38MAPK蛋白的表达有关。

关键词: 血管性痴呆, 养血清脑颗粒, p38丝裂原活化蛋白激酶, 超微结构, 大鼠

Abstract: Objective To observe the effect of Yangxue Qingnao Granule on the ultrastructures and expression of p38 mitogen activated protein kinases (p38MAPK) in CA1 area of hippocampus in vascular dementia rats. Methods 180 Sprague-Dawley rats were randomly divided into sham group, vascular dementia model group (model group) and Yangxue Qingnao Granule treatment group (treatment group). The vascular dementia was modeled with modified Pulsineli's four-vessel occlusion. The ultrastructure of CA1 area was observed with transmission electron microscope, while the expression of p38MAPK in CA1 area was detected with immunohistochemstry and Western blotting 1, 2, 4 and 8 weeks after modeling. Results In the model group, pyknosis, nuclear dissolution, heterochromatin margination and mitochondria swelling were found in most of the neurons in CA1. In the treatment group, the distribution of chromatin was well-proportioned, and mitochondrion and other organelle were normal. In the model group, the expression of p38MAPK increased at each time point compared with the sham group (P<0.01), and peaked 4 weeks after modeling, and decreased in the treatment group compared with the model group (P< 0.01). Conclusion Yangxue Qingnao Granule can improve the ultrastructure of neuronal in CA1 area of hippocampus of vascular dementia rats, which may relate with the inhibition of the expression of p38MAPK.

Key words: vascular dementia, Yangxue Qingnao Granules, p38 mitogen activated protein kinases, ultrastructure, rats