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氧化修饰低密度脂蛋白(Ox—LDL)在动脉粥样硬化发生发展中的作用越来越引起人们的重视。本文通过比较Ox—LDL和脂质过氧化降解产物丙二醛(MDA)修饰的低密度脂蛋白(MDA—LDL)在致泡沫细胞形成方面的差异,探讨了脂质过氧化对巨噬细胞的损伤在泡沫细胞形成中的作用。结果显示:Ox—LDL和MDA—LDL都可被巨噬细胞清道夫受体所识别,引起大量吞噬,造成细胞内胆固醇的聚集,但由MDA—LDL造成的细胞内胆固醇酯聚集可被高密度脂蛋白(HDL_3)所清除,而Ox—LDL造成的胆固醇酯聚集则不能。进一步的研究表明Ox—LDL和MDA—LDL对巨噬细胞HDL_3结合量及细胞内脂质过氧化物(LPO)含量的影响不同。虽然MDA—LDL和Ox—LDL处理巨噬细胞,都可使其HDL_3结合量有不同程度的下降,细胞内LPO含量有不同程度的升高,但当处理因素消除后,细胞继续培养时,由MDA—LDL处理的细胞其降低的HDL_3结合量又有一定的恢复,细胞LPO含量不再上升;而由Ox—LDL处理的细胞,其HDL_3结合量则继续下降,细胞LPO含量则继续升高。由Ox—LDL导致的巨噬细胞HDL_3结合量下降与细胞LPO含量升高之间呈负相关(r=-0.81,P<0.01)。用叔丁基脂氢过氧化物(tbooh)(1×10~(?)mol/L)对巨噬细胞损伤24小时,然后用两种修饰的LDL处理,则两种修饰LDL造成的胆固醇酯聚集都不能被HDL_3清除。本文结果提示Ox—LDL对巨噬细胞的脂质过氧化损伤可能在巨噬细胞向泡沫细胞转变过程中起着重要作用。
The role of Ox-LDL in the development of atherosclerosis has drawn more and more attention. In this paper, we compared the differences in the formation of foam cells between Ox-LDL and malondialdehyde (MDA) -modified low-density lipoprotein (MDA-LDL), and discussed the effect of lipid peroxidation on macrophage The role of damage in foam cell formation. The results showed that both Ox-LDL and MDA-LDL can be recognized by macrophage scavenger receptors, causing massive phagocytosis, resulting in the accumulation of intracellular cholesterol, but the accumulation of intracellular cholesterol esters by MDA-LDL can be blocked by high density Lipoprotein (HDL_3) is cleared, but Ox-LDL cholesterol ester accumulation can not. Further studies showed that Ox-LDL and MDA-LDL had different effects on HDL-3 binding and intracellular lipid peroxidation (LPO) in macrophages. Although MDA-LDL and Ox-LDL treatment of macrophages, HDL_3 binding capacity can have different degrees of decline, intracellular LPO levels have increased to varying degrees, but when the treatment factor is eliminated, the cells continue to culture, from The MDA-LDL-treated cells restored their HDL-3 binding capacity to a certain extent, and the content of LPO did not increase any more. However, the amount of HDL-3 bound by Ox-LDL decreased and the content of LPO increased continuously. There was a negative correlation between the decrease of HDL-3 binding of macrophages induced by Ox-LDL and the increase of cell LPO (r = -0.81, P <0.01). Macrophages were injured for 24 hours with tbooh (1 x 10 ~ (?) Mol / L) and then treated with two modified LDL, then two modified LDL-modified cholesterol esters Aggregation can not be cleared by HDL_3. Our results suggest that oxidative lipid peroxidation of macrophages by Ox-LDL may play an important role in macrophage-to-foam cell transformation.