《中国康复理论与实践》 ›› 2018, Vol. 24 ›› Issue (1): 23-28.doi: 10.3969/j.issn.1006-9771.2018.01.005

• 专题 阿尔茨海默病的干预机制 • 上一篇    下一篇

雷公藤内酯醇对阿尔茨海默病大鼠海马drebrin和cofilin表达的影响

张赛圣1,2, 杨宝林1, 程丽霞3, 万斌1, 聂菁1, 胡小令1, 吕诚1   

  1. 1.南昌大学江西医学院,江西南昌市 330006
    2.十堰市人民医院,湖北十堰市 442000
    3.湖北省东风公司总医院,湖北十堰市 442008
  • 收稿日期:2017-07-24 修回日期:2017-10-03 出版日期:2018-01-25 发布日期:2018-01-31
  • 通讯作者: 吕诚,男,硕士,教授,硕士研究生导师,主要研究方向:老年性痴呆的发病机制及中药实验治疗;E-mail:lvcheng1118@sina.com。
  • 作者简介:张赛圣(1979-),男,汉族,江西抚州市人,硕士,主治医师,主要研究方向:老年性痴呆的发病机制及中药实验治疗。
  • 基金资助:
    1.国家自然科学基金项目(No.81660191; No.30660073); 2.江西省教育厅科研基金项目(No.GJJ150105); 3.江西省卫生计生委科技计划项目(No.20165532)

Effects of Triptolide on Expression of Drebrin and Cofilin in Hippocampus of Rats with Alzheimer's Disease

ZHANG Sai-sheng1,2, YANG Bao-lin1, CHENG Li-xia3, WAN Bin1, NIE Jing1, HU Xiao-ling1, LÜ Cheng1   

  1. 1.Jiangxi Medical College of Nanchang University, Nanchang, Jiangxi 330006, China
    2. Shiyan People's Hospital, Shiyan, Hubei 442000, China
    3. General Hospital of Dongfeng Motor Company, Shiyan, Hubei 442008, China
  • Received:2017-07-24 Revised:2017-10-03 Published:2018-01-25 Online:2018-01-31
  • Contact: LÜ Cheng.E-mail:lvcheng1118@sina.com
  • Supported by:
    National Natural Science Foundation of China (No. 81660191; No. 30660073), Jiangxi Education Department Research Fund (No. GJJ150105) and Jiangxi Health and Family Planning Commission Science and Technology Project (No. 20165532)

摘要: 目的 观察雷公藤内酯醇对阿尔茨海默病(AD)模型大鼠海马神经元drebrin和cofilin表达的影响。方法 雄性Sprague-Dawley大鼠60只随机等分成对照组(n=20)、模型组(n=20)和用药组(n=20)。大鼠右侧海马内注射β淀粉样蛋白(Aβ1-40)造模,对照组右侧海马内注射等量生理盐水。用药组在右侧海马注射Aβ1-40后每天腹腔注射雷公藤内酯醇0.4 mg/kg,共15 d。Golgi染色检测各组海马神经元树突棘密度的变化。免疫组化染色和逆转录聚合酶链反应(RT-PCR)检测各组海马神经元drebrin和cofilin表达的变化。结果 用药组大鼠海马神经元树突棘密度高于模型组(P<0.05)。用药组大鼠海马drebrin阳性产物平均光密度较模型组明显升高(P<0.01),cofilin阳性细胞数和平均光密度较模型组减少(P<0.05)。用药组大鼠海马drebrin mRNA表达高于模型组(P<0.05),cofilin mRNA表达明显低于模型组(P<0.01)。结论 雷公藤内酯醇可能通过调节drebrin和cofilin的表达,延缓AD模型大鼠海马神经元树突棘的退化。

关键词: 阿尔茨海默病, 雷公藤内酯醇, drebrin, cofilin, 大鼠

Abstract: Objective To observe the effects of triptolide on drebrin and cofilin expression in the hippocampus of rats with Alzheimer's disease (AD).Methods Sixty male Sprague-Dawley rats were equally divided into control group, model group and triptolide-treated group with 20 cases in each group. The AD model was established with unilateral injection of beta amyloid 1-40 (Aβ1-40) into hippocampus in rats. The control group was established with unilateral injection of normal saline with the same volume into hippocampus in rats. The triptolide-treated group was administered triptolide intraperitoneally, 0.4 mg/kg, once a day, for 15 days after modeling. Spine density of hippocampal neurons was assayed by Golgi staining. Drebrin and cofilin expression of hippocampal neurons was assayed by immunohistochemical staining and reverse transcription polymerase chain reaction (RT-PCR).Results The spine density of hippocampal neurons was higher in the triptolide-treated group than in the model group (P<0.05). The average optical density of drebrin was higher in the triptolide-treated group than in the the model group (P<0.01), while the cell number and average optical density of cofilin were lower (P<0.05). The drebrin mRNA expression was higher in the triptolide-treated group than in the model group (P<0.05), and the cofilin mRNA expression was lower (P<0.01).Conclusion Triptolide may delay the degeneration of dendritic spines in hippocampal neurons of AD rats by regulating the expression of drebrin and cofilin.

Key words: Alzheimer's disease, triptolide, drebrin, cofilin, rats

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