中国临床解剖学杂志 ›› 2023, Vol. 41 ›› Issue (3): 304-309.doi: 10.13418/j.issn.1001-165x.2023.3.10

• 实验研究 • 上一篇    下一篇

Macamide B促进缺氧缺血性脑损伤新生小鼠神经元的PGRN表达

周倩1,    李莉霞1,    杨晓夏1,    杨俊华1,    文锦坤1,    李朋飞2,    罗利1,    李国营1*   

  1. 1.广东药科大学生命科学与生物制药学院人体解剖学与组织胚胎学系,  广州    510006;    
    2.南方医科大学南方医院妇产科,  广州   510515
  • 收稿日期:2022-11-11 出版日期:2023-05-25 发布日期:2023-06-05
  • 通讯作者: 李国营,教授,硕士生导师,E-mail:gzlgying820@163.com
  • 作者简介:周倩(1998-),女,山西人,在读硕士,主要从事神经损伤修复研究,E-mail:18434875253@163.com
  • 基金资助:
    广东省中医药局科研项目(20212103);广东省医学科学技术研究基金(A2021466);广东普通高校科研项目(2021KQNCX033);国家青年自然科学基金项目(81901524);广东省医学科技研究基金项目(A2020252);广东省自然科学基金(2021A1515011525)

Macamide B promoting the expression of PGRN in hypoxic-ischemic brain damage neonatal mice 

Zhou Qian1, Li Lixia1, Yang Xiaoxia1, Yang Junhua1, Wen Jinkun1, Li Pengfei2, Luo Li1, Li Guoying1*   

  1. 1. Department of Human Anatomy and Histoembryology, School of Life Sciences and Biopharmaceutics, Guangdong Pharmaceutical University, Guangzhou 510006, China; 2. Department of Obstetrics and Gynecology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China
  • Received:2022-11-11 Online:2023-05-25 Published:2023-06-05

摘要: 目的    研究玛咖酰胺B(Macamide B)对缺氧缺血性脑损伤(hypoxic-ischemic brain damage,HIBD)的新生小鼠神经元中颗粒蛋白前体(Progranulin,PGRN)及糖氧剥夺(oxygen-glucose deprivation,OGD)后的小鼠海马神经元细胞系(HT22)中PGRN表达的影响,探究Macamide B在新生小鼠HIBD后发挥神经保护作用的机制。  方法    建立HIBD小鼠模型,将出生后7 d的C57小鼠随机分为Sham组、HIBD组和Macamide B组;HT22细胞培养并制备OGD细胞模型,分为Control组、OGD组和Macamide B组。通过免疫荧光、Western blot检测小鼠神经元或HT22细胞中PGRN的表达。  结果    体内实验显示,与Sham组相比,HIBD组小鼠神经元中PGRN表达降低;与HIBD组相比,Macamide B组小鼠神经元中PGRN表达升高。在体外,与Control组相比,OGD组HT22细胞中PGRN表达降低;与OGD组相比,Macamide B组HT22细胞中PGRN表达显著升高。  结论    Macamide B可能通过促进PGRN表达对HIBD新生小鼠发挥神经保护作用。

关键词: 缺氧缺血性脑损伤; ,  , Macamide B; ,  , 神经保护; ,  , PGRN

Abstract: Objective    To investigate the effect of Macamide B on the expression of progranulin (PGRN) in neurons of neonatal mice with hypoxic-ischemic brain damage (HIBD) and HT22 mouse hippocampal neuron cell line after oxygen-glucose deprivation (OGD) and explore the mechanism of the neuroprotective effect of Macamide B after HIBD in neonatal mice.    Methods    The HIBD model of C57 mice was established after 7 days of birth and the mice were divided into Sham group, HIBD group and Macamide B group. HT22 cells were cultured, then the OGD model of HT22 cells was established, and the cells were divided into Control group, OGD group and Macamide B group. The expression of PGRN in mouse neurons or HT22 cells was detected by immunofluorescence staining and Western blot.    Results     In vivo experiments showed that compared with Sham group, the expression of PGRN in mice neurons of HIBD group was reduced. Compared with HIBD group, the expression of PGRN in neurons of Macamide B group was increased. In vitro, compared with Control group, the expression of PGRN in HT22 cells of OGD group was decreased. Compared with OGD group, the expression of PGRN in HT22 cells of Macamide B group rose significantly.    Conclusions     Macamide B may play a neuroprotective role in HIBD neonatal mice by promoting the expression of PGRN.

Key words: Hypoxic-ischemic brain damage; ,  ,  Macamide B; ,  ,  Neuroprotection; ,  , PGRN

中图分类号: