中文摘要：

为研究低密度脂蛋白（LDL）、氧化修饰的低密度脂蛋白（oxLDL）对THP-1源性巨噬细胞中PCSK9、LDLR表达的影响及两者之间的关系.分别用0mg/L、10mg/L、20mg/L、30mg/L的LDL和0mg/L、10mg/L、20mg/L、30mg/L的oxLDL处理THP-1巨噬细胞,油红O染色检测细胞荷脂情况,免疫荧光检测THP-1巨噬细胞上PCSK9蛋白表达及分布情况,RT-PCR、Western blot检测THP-1巨噬细胞上PCSK9、LDLR mRNA、蛋白质的表达.结果发现,不同浓度LDL处理THP-1巨噬细胞后,随着LDL浓度的增大,细胞内脂滴数目略有增多.免疫荧光染色发现,PCSK9在THP-1巨噬细胞上的表达随LDL浓度的增加而增多,胞浆内定位于某一特定细胞器中;RT-PCR、Western blot检测发现,LDL可以呈浓度依赖性下调THP-1巨噬细胞中LDLR的表达和上调PCSK9的表达.不同浓度oxLDL处理THP-1巨噬细胞后,随oxLDL浓度的增大,脂滴颗粒明显增加;oxLDL处理对THP-1巨噬细胞上PCSK9、LDLR mRNA、蛋白质的表达影响均不明显.研究结果表明：THP-1巨噬细胞上,同时有PCSK9和LDLR的表达,且PCSK9定位于胞浆中某一特定细胞器;oxLDL对THP-1巨噬细胞LDLR和PCSK9表达没有影响;LDL能够降低THP-1巨噬细胞表面LDLR的表达,同时上调PCSK9表达,初步说明在THP-1巨噬细胞中,两者有一定的相关性.

英文摘要：

In order to study the effects of LDL and oxLDL on expression of PCSK9 and LDLR in THP-1 macrophages and find the relationship between them. THP-1 cells were induced to differentiate into macrophages by PMA treatment. Cells were then co-incubated with LDL or oxLDL with a concentration of 0 mg/L, 10 mg/L, 20 mg/L, 30 mg/L for 24h respectively. Cellular lipid was visualized by oil red O staining. The localization and semiquantitation of PCSK9 was confirmed by immunofluorescence assay, the expression of PCSK9 and LDLR was analyzed by RT-PCR and Western blotting. Oil red O staining showed that a number of visualized lipid droplet accumulated within THP-1 cells. The lipid droplet is big and accumulating in cells co-incubated with oxLDL but small and dispersing when co-incubated with LDL. Matured PCSK9 are expressed on the cell surface and some organelle, and increased with the increasing of LDL concentration through immunofluorescence assay. RT-PCR, Western blot showed that, in THP-1 , LDLR was downregulated while PCSK9 was upregulated especially when treated with LDL, but the treatment of low concentration of oxLDL likely had no effect on expression of LDLR and PCSK9. Together, these results reveal that PCSK9 and LDLR may co-expressed in THP-1 cells, which are unable to be influenced by oxLDL, but may be down-regulated （LDLR） or up-regulated （PCSK9） by LDL, providing primary evidence of the correlation between PCSK9 and LDLR.