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15-羟基二十碳四烯酸促肺动脉平滑肌细胞增殖的研究

发布时间:2018-11-23 10:00
【摘要】:目的:研究缺氧条件下15-羟基二十碳四烯酸(15-HETE)对兔肺动脉平滑肌细胞增殖的影响 方法:培养日本大耳白兔肺动脉平滑肌细胞(PASMC),Western blotting检测Phospho-ERK1/2、ERK1/2、Phospho-p38MAPK及p38MAPK的表达。通过应用四噻唑蓝比色法(MTT)及Brdu法观察MEK阻断剂U0126及p38MAPK阻断剂SB202190以及15-HETE在缺氧情况下对肺动脉平滑肌细胞增殖的影响及可能机制。 结果:缺氧使兔肺动脉平滑肌细胞发生增殖并且上调15-LO的表达,,15-HETE可促进兔肺动脉平滑肌细胞增殖并且激活Phospho-ERK1/2的表达,ERK1/2未发生明显变化。加入MEK阻断剂U0126后细胞的增殖作用受到了阻断。 结论:缺氧条件下15-HETE促进兔肺动脉平滑肌细胞增殖与MAPK家族中的ERK1/2信号转导通路有关。
[Abstract]:Objective: to study the effect of 15-hydroxy-icosapentaenoic acid (15-HETE) on the proliferation of rabbit pulmonary artery smooth muscle cells under hypoxia. Methods: Phospho-ERK1/2, was detected by (PASMC), Western blotting in cultured rabbit pulmonary artery smooth muscle cells. Expression of ERK1/2,Phospho-p38MAPK and p38MAPK. The effects of MEK blocker U0126, p38MAPK blocker SB202190 and 15-HETE on the proliferation of pulmonary artery smooth muscle cells under hypoxia were observed by (MTT) and Brdu assay with tetrathiazolyl blue colorimetry. Results: hypoxia induced proliferation of rabbit pulmonary artery smooth muscle cells and up-regulated the expression of 15-LO. 15-HETE promoted the proliferation of rabbit pulmonary artery smooth muscle cells and activated the expression of Phospho-ERK1/2. ERK1/2 did not change significantly. The proliferation of U0126 cells was blocked by the addition of MEK blocker U0126. Conclusion: the proliferation of rabbit pulmonary artery smooth muscle cells stimulated by 15-HETE under hypoxia is related to the ERK1/2 signal transduction pathway in the MAPK family.
【学位授予单位】:哈尔滨医科大学
【学位级别】:硕士
【学位授予年份】:2012
【分类号】:R329.2

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相关期刊论文 前4条

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