首页  期刊介绍 征稿简则 编委会 期刊征订 广告服务 留言板 联系我们 English

中国应用生理学杂志 ›› 2022, Vol. 38 ›› Issue (5): 480-484.doi: 10.12047/j.cjap.6269.2022.090

• 研究论文 • 上一篇    下一篇

丁苯酞对睡眠剥夺大鼠脑额叶HMGB1和RAGE表达的影响*

杨滢霞1, 郭育芬2, 黄红红1, 王凌星1△   

  1. 1.福建医科大学附属第二医院神经内科, 泉州 362000;
    2.厦门市湖里区妇幼保健院健康教育科, 厦门 361000
  • 收稿日期:2022-02-14 修回日期:2022-08-14 出版日期:2022-09-28 发布日期:2023-04-23
  • 通讯作者: Tel: 18965610722; E-mail: lxing502@fjmu.edu.cn
  • 基金资助:
    *福建省自然科学基金项目(2019J01471); 泉州市高层次人才创新创业项目(2018C050R);福建省卫生健康青年科研课题(2020QNB030)

Effects of Butylphthalide on the expressions of HMGB1 and RAGE in frontal lobe of rats after chronic sleep deprivation

YANG Ying-xia1, GUO Yu-fen2, HUANG Hong-hong1, WANG Ling-xing1△   

  1. 1. Department of Neurology, Second Affiliated Hospital of Fujian Medical University, Quanzhou 362000;
    2. Department of Health Education, XiamenHuli District Maternity and Child Care Hospital, Xiamen 361000, China
  • Received:2022-02-14 Revised:2022-08-14 Online:2022-09-28 Published:2023-04-23

摘要: 目的: 探讨丁苯酞对睡眠剥夺大鼠脑额叶高迁移率族蛋白1(HMGB1)和晚期糖基化终产物受体(RAGE)表达的影响。方法: 建立Sprague Dawley(SD)大鼠慢性睡眠剥夺和丁苯酞干预模型,共分为3组(n=6):大平台对照组、慢性睡眠剥夺组、慢性睡眠剥夺+丁苯酞组,慢性睡眠剥夺组采用睡眠剥夺箱对大鼠进28 d,18 h/d的睡眠剥夺,慢性睡眠剥夺+丁苯酞组在睡眠剥夺28 d后腹腔注射丁苯酞100 mg/(kg·d),共14 d。各组大鼠取脑部标本,免疫组化检测额叶高迁移率族蛋白1 (HMGB1)、核转录因子kappB(NF-κB) p65表达,Western blot检测大鼠额叶HMGB1、沉默信息调节因子1(SIRT1)、晚期糖基化终产物(RAGE)、NF-κB表达。结果: 与大平台对照组比较,慢性睡眠剥夺组大鼠额叶HMGB1、RAGE、细胞核NF-κBp65表达显著增多(P均<0.05),而SIRT1表达显著减少(P<0.05);与慢性睡眠剥夺组比较,慢性睡眠剥夺+丁苯酞组大鼠额叶HMGB1、RAGE、细胞核NF-κBp65表达显著减少(P均<0.05),而SIRT1表达显著增加(P<0.05)。结论: 丁苯酞可通过改变慢性睡眠剥夺大鼠额叶HMGB1和RAGE表达,减少NF-κBp65的核转移,抑制额叶HMGB1/RAGE/NF-κB信号通路。

关键词: 慢性睡眠剥夺, 丁苯酞, 高迁移率族蛋白, 晚期糖基化终产物, 大鼠

Abstract: Objective: To investigate the effects of Butylphthalide on the expressions of HMGB1 and RAGE in frontal lobe of rats after chronic sleep deprivation. Methods: Chronic sleep deprivation and butylphthalide treatment was performed in Sprague Dawley(SD)rats and the rats were divided into three groups (n=6): platform control group, chronic sleep deprivation group and chronic sleep deprivation + butylphthalide intervention group. Rats suffering chronic sleep deprivation were put in multiple platforms box for 18 h per day and sleep deprivation lasted for 28 days. Rats in butylphthalide intervention group were intraperitoneally injected with butylphthalide 100 mg/(kg·d) for 14 days after sleep deprivation. After collecting brains, high-mobility group box (HMGB1) and nuclear transcription factor kappB (NF-κB)p65 were detected by immunohistochemistry. The expression of HMGB1, silent information regulator of transcription 1 (SIRT1), receptor for advanced glycation end-products (RAGE) and NF-κB in frontal lobe were determinated by Western blot. Results: Compared with platform control group, the expression levels of HMGB1, RAGE and nuclear NF-κB p65 were increased significantly, while the expression of SIRT1 was decreased siginificantly in frontal lobe of chronic sleep deprivation group (all P<0.05). Compared with chronic sleep deprivation group, the expression levels of of HMGB1, RAGE and nuclear NF-κB p65 were decreased significantly, while the expression of SIRT1 was increased significantly in chronic sleep deprivation + butylphthalide intervention group (all P<0.05). Conclusion: Butylphthalide can inhibit HMGB1/RAGE/NF-κB pathway in frontal lobe of rats after chronic sleep deprivation by changing the expression of HMGB1 and RAGE, and reducing the nuclear translocation of NF-κBp65.

Key words: chronic sleep deprivation, butylphthalide, HMGB1, RAGE, rats

中图分类号: 

版权所有 © 2015 《中国应用生理学杂志》编辑部
京ICP备16058274号-1
地址:天津市和平区大理道1号,邮编:300050  电话:022-23909086  E-mail:editor@cjap.ac.cn
本系统由北京玛格泰克科技发展有限公司设计开发 技术支持:support@magtech.com.cn