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目的:研究脂蛋白a(lipoprotein a,Lpa)在终末期肾病(end-stage renal disease,ESRD)动脉粥样硬化中的作用,并进一步探讨CXC趋化因子配体16(CXC chemokine ligand 16,CXCL16)和低密度脂蛋白受体(low density lipoprotein receptor,LDLr)是否介导了Lpa的胞内摄入。方法:根据血浆Lpa质量浓度将46例ESRD患者分为对照组[ρ(Lpa)<300 mg·L~(-1),n=23]和高Lpa组[ρ(Lpa)≥300 mg·L~(-1),n=23]。检测两组患者的生化指标和脂质谱。取ESRD患者动静脉内瘘手术时桡动脉边缘切除的组织,HE染色观察其泡沫细胞形成、Filipin染色观察其胆固醇沉积;免疫组化和免疫荧光染色观察其Lpa的沉积;免疫组化观察LDLr和CXCL16的表达;免疫荧光共染分别观察Lpa和LDLr、Lpa和CXCL16的共表达。结果:与对照组比较,高Lpa组ESRD患者的桡动脉中泡沫细胞增多、胆固醇沉积增加、Lpa沉积增加、CXCL16和LDLr表达增加(均P<0.05);相关性分析显示,血浆Lpa质量浓度与Lpa沉积程度(r=0.72,P<0.01)、LDLr表达(r=0.54,P<0.01)、CXCL16表达(r=0.6,P<0.01)均呈正相关。进一步免疫荧光共染发现,高Lpa组的桡动脉组织中Lpa与LDLr、CXCL16共表达均增加(均P<0.05)。结论:Lpa在ESRD患者桡动脉中沉积,促进泡沫细胞形成,进而导致动脉粥样硬化的发生,LDLr和CXCL16可能是介导Lpa进入桡动脉组织细胞内的主要脂蛋白受体。
OBJECTIVE: To study the role of lipoprotein a (Lpa) in the treatment of atherosclerosis in end-stage renal disease (ESRD) and to further explore the role of CXC chemokine ligand 16 (CXCL16 ) And low density lipoprotein receptor (LDLr) mediated the intracellular uptake of Lpa. Methods: 46 patients with ESRD were divided into control group (ρ (Lpa) <300 mg · L -1, n = 23] and ρ (Lpa) ≥300 mg · L ~ (-1), n = 23]. Biochemical parameters and lipid profile were measured in both groups. The tissues of the radial artery resected at the time of arteriovenous fistula surgery were obtained from ESRD patients. The formation of foam cells was observed by HE staining and the deposition of cholesterol by Filipin staining. The deposition of Lpa was observed by immunohistochemistry and immunofluorescence staining. CXCL16 expression; immunofluorescence co-staining were observed Lpa and LDLr, Lpa and CXCL16 co-expression. RESULTS: Compared with the control group, the number of foam cells in the radial artery increased, the deposition of cholesterol increased, the deposition of Lpa increased and the expressions of CXCL16 and LDLr increased in ESRD patients (all P <0.05). The correlation analysis showed that plasma Lpa concentration and Lpa deposition (r = 0.72, P <0.01), LDLr expression (r = 0.54, P <0.01) and CXCL16 expression (r = 0.6, P <0.01). Further immunofluorescence co-staining showed that the co-expression of Lpa, LDLr and CXCL16 in radial artery tissue of high Lpa group were increased (all P <0.05). CONCLUSION: Lpa deposits in the radial artery of ESRD patients and promotes the formation of foam cells, leading to atherosclerosis. LDLr and CXCL16 may be the major lipoprotein receptors that mediate Lpa entry into radial artery tissue.