PDE4B2在LPS诱导的炎症反应信号通路中的作用研究
基本信息
结项摘要
磷酸二酯酶4（PDE4）为cAMP水解通路的唯一代谢酶，又分为A、B、C、D四亚型。已有的研究表明PDE4B与LPS诱导的TNF-alpha的产生有重要作用。PDE4B基因敲除小鼠的研究表明PDE4B（-/-）小鼠对LPS诱导的休克耐受力明显提高，且LPS刺激腹腔巨型噬细胞分泌TNF-alpha明显下降。我们的前期研究也证实PDE4抑制剂对LPS诱导的大鼠急性肺损伤有明显的保护作用，且PDE4活性与TNF-alpha活性的升高呈平行关系。PDE4B2是PDE4亚型中唯一的短形，已有的研究表明PDE4B2对LPS诱导的TNFalpha产生有关键作用。但PDE4B2如何发挥作用尚不清楚。因此，我们拟以PDE4B基因敲除小鼠和稳定转染PDE4B2-SiRNA 单核细胞株U937为研究对象，以LPS诱导的炎症反应正负反馈调节信号通路为主线，研究并阐明PDE4B2在LPS诱导的炎症信号通路中的作用。
项目摘要
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数据更新时间：2023-05-31
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