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  • 曹帆帆,徐莉敏,王莹,等.雷公藤红素对β淀粉样蛋白诱导SH-SY5Y细胞Tau蛋白异常磷酸化影响的研究[J].同济大学学报(医学版),2016,37(4):36-39, 50.    [点击复制]
  • CAO Fan-fan,XU Li-min,WANG Ying,et al.Effects of Tripterine on Tau hyperphosphorylation induced by β-amyloid peptides in cultured SH-SY5Y cells[J].同济大学学报(医学版),2016,37(4):36-39, 50.   [点击复制]
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雷公藤红素对β淀粉样蛋白诱导SH-SY5Y细胞Tau蛋白异常磷酸化影响的研究
曹帆帆,徐莉敏,王莹,彭彬,张雪,张登海
0
(第二军医大学附属公利医院中法合作中心实验室,上海 200135;第二军医大学附属公利医院检验科,上海 200135)
摘要:
观察雷公藤红素对β淀粉样蛋白142导致SHSY5Y细胞Tau蛋白异常磷酸化的影响及其可能机制。〖HT5”H〗方法〖HT5”K〗用 Aβ142刺激SHSY5Y细胞,建立Tau蛋白异常磷酸化的细胞模型。加入雷公藤红素干预,Western印迹法检测Aβ142导致Tau蛋白异常磷酸化的变化,同时检测pNFSymbolkA@B表达情况;siRNA法下调TLR4表达,Western印迹法检测Aβ142导致的Tau蛋白异常磷酸化的变化情况;同时观察下调TLR4后,Aβ142刺激对pNFSymbolkA@B表达的影响。〖HT5”H〗结果〖HT5”K〗Aβ142刺激SHSY5Y细胞,导致Tau蛋白Ser199/202、Ser396位点的磷酸化水平增加,而雷公藤红素能降低这两个位点磷酸化水平;Aβ142导致细胞pNFSymbolkA@B表达增加,雷公藤红素干预后pNF SymbolkA@B表达下调,且NFSymbolkA@B抑制剂BAY117082同样能降低Aβ142导致的Tau蛋白异常磷酸化;下调TLR4表达,Aβ142导致的Tau蛋白异常磷酸化及pNFSymbolkA@B表达下降。〖HT5”H〗结论〖HT5”K〗雷公藤红素降低Aβ142导致的SH SY5Y细胞Tau蛋白异常磷酸化可能与其抑制TLR4/NF SymbolkA@ B通路活性有关。
关键词:  雷公藤红素  β淀粉样蛋白  Tau蛋白  Toll样受体4  pNFSymbolkA@B
DOI:10.16118/j.1008-0392.2016.04.007
投稿时间:2016-04-18
基金项目:上海市浦东新区卫生系统优秀青年医学人才培养计划(PWRq2013-11);上海市青年科技英才扬帆计划(15YF1410800)
Effects of Tripterine on Tau hyperphosphorylation induced by β-amyloid peptides in cultured SH-SY5Y cells
CAO Fan-fan,XU Li-min,WANG Ying,PENG Bin,ZHANG Xue,ZHANG Deng-hai
(Sino-French Cooperative Central Lab, Shanghai Gongli Hospital, the Second Military Medical University, Shanghai 200135, China;Clinical laboratory, Shanghai Gongli Hospital, the Second Military Medical University, Shanghai 200135, China)
Abstract:
Objective To investigate the effects and mechanisms of tripterine on Tau hyperphospho rylation induced by β amyloid in SH SY5Y cells. Methods The effects of tripterine on the changes of Tau hyperphosphorylation and p NF SymbolkA@B induced by βamyloid in SHSY5Y cells were measured by Western blotting after TLR4 knocking down by siRNA. ResultsCompared with the control group, the expressions of Tau pSer199/202 and pSer396 were markedly increased after the induction of Aβ142, while the hyperphosphorylation of Tau pSer199/202 and pSer396 induced by Aβ142 was decreased by tripterine. The increasing of pNFSymbolkA@B expression induced by Aβ142was decreased after the treatment of tripterine, and NFSymbolkA@B inhibitor BAY117082 also decreased the hyperphosphorylation of Tau pSer199/202 and pSer396 induced by Aβ142. The hyperphosphorylation of Tau pSer199/202 and pSer396 and pNFSymbolkA@B expression induced by Aβ142 was decreased after knocking down TLR4. ConclusionDecreasing of Tau hyperphosphorylation by Tripterine is partially via inhibiting the TLR4/NFSymbolkA@B signaling pathway.
Key words:  tripterine  βamyloid  Tau  Toll like receptor 4  pNF SymbolkA@B

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