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岭南现代临床外科 ›› 2019, Vol. 19 ›› Issue (01): 34-43.DOI: 10.3969/j.issn.1009-976X.2019.01.007

• 论著与临床研究 • 上一篇    下一篇

棕榈酸与脂多糖协同促进主动脉平滑肌细胞MCP?1的表达

宋自姣1,2, 刘珊英2, 林灿祥2,3, 李焱1*   

  1. 中山大学孙逸仙纪念医院 1.内分泌科;2.广东省恶性肿瘤表观遗传和基因调控重点实验室;3.心胸外科,广州 510120
  • 通讯作者: 李焱
  • 基金资助:
    国家自然科学基金

Palmitic acid and LPS cooperatively promote MCP-1 expression in aortic smooth muscle cells

Zijiao1,2, LIU Shanying2, LIN Canxiang2,3, LI Yan1   

  1. 1. Department of Endocrinology; 2. Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation; 3. Department of Cardiothoracic Surgery, Sun Yat?sen Memorial Hospital, Sun Yat?sen University, Guangzhou 510120, China
  • Online:2019-02-20 Published:2019-02-20
  • Contact: LI Yan
  • Supported by:
    The National Natural Science Fund

摘要: [摘要] 目的 研究棕榈酸及脂多糖(LPS)对主动脉平滑肌细胞MCP?1表达的影响及可能的机制。方法 使用棕榈酸和(或)LPS对大鼠胸主动脉平滑肌细胞(A7r5) 处理24 h后, 应用RT?qPCR、ELISA法检测MCP?1表达及应用RT?qPCR和Western Blotting法检测toll样受体4(TLR4)表达情况;细胞在TLR4抑制剂(TAK?242)预处理1 h后加入棕榈酸和(或)LPS处理24 h,检测MCP?1表达情况。结果 使用棕榈酸和(或)LPS处理的A7r5细胞,其MCP?1 mRNA表达水平和蛋白质分泌增加,LPS增强由棕榈酸诱导的MCP?1的表达;棕榈酸和LPS均可上调TLR4蛋白质表达,两者同时作用于A7r5细胞时,TLR4蛋白表达水平进一步升高;TAK242(5 μM)处理A7r5细胞后,棕榈酸及LPS诱导的MCP?1蛋白分泌减少。结论 棕榈酸与LPS通过TLR4协同促进主动脉平滑肌细胞MCP?1表达,参与动脉粥样硬化病变过程。

关键词: 单核细胞趋化因子1, 平滑肌细胞, 棕榈酸, 脂多糖, toll样受体4

Abstract: [Abstract] Objective To investigate the effects of palmitic acid and lipopolysaccharide (LPS) on the expression of MCP?1, and to explore the involving underlying molecular mechanisms in rat thoracic aortic smooth muscle A7r5 cell line. Methods After the A7r5 cells were respectively incubated for 24 h with 0.2% BSA, palmitic acid (200 μM) , LPS (1 μg/ml)+0.2% BSA and palmitic acid (200 μM ) +LPS (1 μg/ml), MCP?1 was detected by the methods of RT?qPCR and ELISA and toll?like receptor 4 (TLR4 ) was determined by the methods of RT?qPCR and Western Blotting. Moreover, palmitic acid?induced MCP?1 was further detected after the pre?treatment with TAK?242, a toll?like receptor 4 inhibitor. Results Both palmitic acid and LPS had increase the mRNA and protein of MCP?1 in A7r5 cells, while the result of palmitic acid co?treatment with LPS showed MCP?1 was significantly enhanced when comparing with the single treatment. Palmitic acid and LPS upregulated TLR4 in the expression of protein, but not mRNA. Moreover, TAK?242 blocked the MCP?1 induced by LPS, which partially exerted the similar inhibiting effects on the palmitic acid?induced MCP?1. Conclusion Both palmitic acid and LPS can increase the production of MCP?1 via TLR4 and the synergy treatment of LPS with palmitic acid aggravated MCP?1 in thoracic aorta smooth muscle cells, which may play a potential role in the progression of atherosclerosis.

Key words: lipopolysaccharide, smooth muscle cell, palmitic acid, toll?like receptor 4, monocyte chemotactic protein 1

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