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中国应用生理学杂志 ›› 2018, Vol. 34 ›› Issue (5): 385-388.doi: 10.12047/j.cjap.5668.2018.088

• 研究论文 •    下一篇

TGF-β1对Aβ1-42诱导海马神经元-小胶质细胞共培养体系中细胞因子表达和分泌的影响

方小霞1,2, 周易1, 孙高林1, 邱一华1, 彭聿平1   

  1. 1. 南通大学医学院生理学系, 江苏 南通 226001;
    2. 南通大学机能学实验室, 江苏 南通 226001
  • 收稿日期:2018-01-05 修回日期:2018-08-02 出版日期:2018-09-28 发布日期:2019-02-21
  • 通讯作者: 彭聿平,Tel:86-0513-85051714;E-mail:yppeng@ntu.edu.cn E-mail:yppeng@ntu.edu.cn
  • 基金资助:
    国家自然科学基金项目(31371182);江苏省高等学校自然科学研究面上项目(18KJD310003);江苏省教育厅研究生科研与实践创新计划项目(KYCX18_2399)

Effects of TGF-β1 on the expression and secretion of cytokines induced by Aβ1-42 in hippocampal neuron and microglia co-cultures

FANG Xiao-xia1,2, ZHOU Yi1, SUN Gao-lin1, QIU Yi-hua1, PENG Yu-ping1   

  1. 1. Department of Physiology, School of Medicine, Nantong University, Nantong 226001, China;
    2. Function Laboratory, School of Medicine, Nantong University, Nantong 226001, China
  • Received:2018-01-05 Revised:2018-08-02 Online:2018-09-28 Published:2019-02-21
  • Supported by:
    国家自然科学基金项目(31371182);江苏省高等学校自然科学研究面上项目(18KJD310003);江苏省教育厅研究生科研与实践创新计划项目(KYCX18_2399)

摘要: 目的:探讨在海马神经元和小胶质细胞共培养体系中转化生长因子-β1(TGF-β1)对β淀粉样肽1-42(Aβ1-42)诱导的小胶质细胞激活表达和分泌细胞因子的影响。方法:将大鼠海马神经元和小胶质细胞进行共同培养,于共同培养后第5日,加入TGF-β1(5 or 20 ng/ml),1 h后加入Aβ1-42(5 μmol/L),继续培养72 h后用于后续实验,Western blot法检测诱导型一氧化氮合酶(iNOS)的蛋白表达;Real-time PCR和ELISA法检测肿瘤坏死因子-α(TNF-α)、白介素-1β(IL-1β)和胰岛素样生长因子(IGF-1)的mRNA表达和分泌。结果:在共同培养的海马神经元与小胶质细胞体系中,Aβ1-42诱导炎症因子iNOS、TNF-α和IL-1β的表达和/或分泌上调,神经营养因子IGF-1表达下调,TGF-β1预处理削弱上述Aβ1-42的作用。结论:TGF-β1明显抑制Aβ1-42诱导的小胶质细胞激活引起的炎性细胞因子的增加和神经营养因子的减少。

关键词: TGF-β1, 1-42, 小胶质细胞, 海马神经元, 细胞因子

Abstract: Objective: To investigate the neuroprotective effects of transforming growth factor beta 1(TGF-β1) on the expression and secretion of cytokines induced by Aβ1-42 in hippocampal neurons and microglial co-cultures. Methods: Hippocampal neurons and microglia obtained from SD rat were co-cultured. TGF-β1 was applied on day 5 after the neurons and microglia co-cultures were incubated at the concentrations of 5 or 20 ng/ml, Aβ1-42 was added 1 h following TGF-β1 application at a concentration of 5 μmol/L. They were incubated for 72 h and then assessed for further studies. Western blot analyses were employed to examine the expression of inducible nitric oxide synthase (iNOS); Real-time PCR and ELISA were used to detect the mRNA expression and secretion of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and insulin-like growth factor-1 (IGF-1). Results: In the hippocampal neuron-microglia co-cultures, Aβ1-42 induced upregulation of iNOS, TNF-α and IL-1β, downregulation of IGF-1. TGF-β1 pretreatment ameliorated the pro-inflammatory effects caused by Aβ1-42. Conclusion: TGF-β1 significantly inhibits the increase in inflammatory cytokines and the decrease in neurotrophic factor which are caused by Aβ1-42-induced microglia activation.

Key words: TGF-β1, 1-42, microglia, hippocampal neurons, cytokines

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