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目的探讨宁心痛颗粒含药血清及主要药物的有效组分(黄芪多糖、藁本内酯)干预THP-1源性巨噬细胞泡沫化的效应与机制。方法采用佛波酯诱导人THP-1细胞转化为巨噬细胞,再与oxLDL共培养建立泡沫细胞模型;分为空白对照组、模型对照组、宁心痛颗粒含药血清(CMS)组、空白血清组、黄芪多糖(APS)组、藁本内酯(LIG)组、黄芪多糖合藁本内酯(APS+LIG)组7组,对巨噬细胞泡沫化过程进行干预。运用高效液相色谱法检测泡沫化程度(CE/TC比值),Western blot法检测SRA-Ⅰ、CD36、ABCA1、LXR-α、PPAR-γ的表达。结果与空白对照组比较,模型对照组CE/TC值、SRA-Ⅰ、CD36、ABCA1及LXR-α、PPARγ蛋白表达升高(P<0.05);与模型对照组比较,LIG组、APS+LIG组、CMS组CE/TC值降低(P<0.05),除APS组ABCA1外,APS组、LIG组、APS+LIG组、CMS组SRA-Ⅰ、CD36蛋白表达降低,ABCA1、LXR-α、PPARγ蛋白表达升高(P<0.05)。与APS组比较,CMS组CE/TC值降低,ABCA1蛋白表达升高(P<0.05)。结论宁心痛颗粒含药血清、主要药物的有效组分(APS、LIG)均可不同程度抑制THP-1源性巨噬细胞泡沫化,其机制可能与调节巨噬细胞脂质吞噬-逆转运间的平衡,即下调脂蛋白吞噬受体SRA-Ⅰ、CD36的表达,上调胆固醇逆转运通路中的ABCA1、PPARγ及LXR-α的表达有关。
Objective To investigate the effect and mechanism of Ningxintong Granule containing medicated serum and main active ingredients (Astragalus Polysaccharides, ligustilide) on the foaming of THP-1-derived macrophages. Methods Phosphatidylinositol induced human THP-1 cells into macrophages, then co-cultured with oxLDL to establish a foam cell model; divided into blank control group, model control group, Ningxin Tong granule containing serum (CMS) group, blank serum (APS) group, ligustilide (LIG) group and APS + LIG group (7 groups). The intervention of macrophage foam process was carried out. The degree of foaming (CE / TC ratio) was measured by high performance liquid chromatography. The expression of SRA-Ⅰ, CD36, ABCA1, LXR-α and PPAR-γ was detected by Western blot. Results Compared with the blank control group, the expression of CE / TC, SRA-Ⅰ, CD36, ABCA1 and LXR-α and PPARγ in the model control group were significantly increased (P <0.05). Compared with the model control group, The levels of CEA and TC in CMS group decreased (P <0.05). In addition to ABCA1 in APS group, the expression of SRA-Ⅰ and CD36 in APS group, LIG group, APS + LIG group and CMS group decreased, while ABCA1, LXR-α and PPARγ The protein expression increased (P <0.05). Compared with APS group, CE / TC decreased and ABCA1 protein increased in CMS group (P <0.05). Conclusions Ningxintong Granule contains the serum and the active ingredients of main drugs (APS, LIG) can inhibit the foaming of THP-1-derived macrophages to varying degrees. The mechanism may be related to the regulation of macrophage lipophilic phagocytosis- , That is, the down-regulation of lipoprotein phagocytic receptors SRA-Ⅰ and CD36, and up-regulation of ABCA1, PPARγ and LXR-α in cholesterol reverse transport pathway.