LOX-1在动脉粥样硬化中的作用研究新进展

动脉粥样硬化(AS)是一种血管慢性炎症性病变,其中内皮细胞功能异常、单核细胞的黏附和迁移、平滑肌细胞的凋亡、泡沫细胞的形成和血小板的活化是AS形成的关键环节,最终结果是形成大、中动脉内膜下的粥样硬化斑块,造成管腔狭窄,远端组织器官供血不足甚至栓塞。低密度脂蛋白（LDL） 氧化形成的氧化型LDL（ox-LDL）在AS发生、发展过程中起着重要作用。目前在与AS发生、发展相关的细胞（如血管内皮细胞、血管平滑肌细胞、单核细胞、巨噬细胞以及泡沫细胞）上已经发现和鉴定了多种oxLDL受体,其中瘦素样氧化型低密度脂蛋白受体(LOX)-1表达于血管内皮细胞、巨噬细胞、血小板上,是ox-LDL的主要受体［1］,在AS的发生、发展中起着重要作用,本文将着重阐述近年来LOX-1影响AS发生发展相关效应与机制的新进展。     

CD36 and macrophages in atherosclerosis

CD36 is a multi-ligand scavenger receptor present on the surface of a number of cells such as platelets, monocytes/macrophages, endothelial and smooth muscle cells. Monocyte/macrophage CD36 has been shown to play a critical role in the development of atherosclerotic lesions by its capacity to bind and endocytose oxidized low density lipoproteins (OxLDL), and it is implicated in the formation of foam cells. However, the significance of CD36 in atherosclerosis has recently been called into question by different studies, and therefore its exact role still needs to be clarified. The aim of this article is to carefully review the importance of CD36 as an essential component in the pathogenesis of atherosclerosis.     

异鼠李素通过抑制泡沫细胞形成增加动脉粥样硬化斑块稳定性的机制研究

背景 泡沫细胞的形成是动脉粥样硬化重要的病理基础,其是由巨噬细胞吞噬大量胆固醇和三酰甘油后转化而来.因此,如何促进巨噬细胞的脂质代谢、抑制其转化为泡沫细胞是延缓动脉粥样硬化病情进展的关键.目的 分析异鼠李素通过抑制泡沫细胞形成增加动脉粥样硬化斑块稳定性的机制.方法 本实验时间为2020年8月至2021年10月.动物实验...     

Current Concepts of the Role of Oxidized LDL Receptors in Atherosclerosis

Atherosclerosis is characterized by accumulation of lipids and inflammatory cells in the arterial wall. Oxidized low-density lipoprotein (ox-LDL) plays important role in the genesis and progression of atheromatous plaque. Various scavenger receptors have been recognized in the past two decades that mediate uptake of ox-LDL leading to formation of foam cells. Inhibition of scavenger receptor A and CD36 has been shown to affect progression of atherosclerosis by decreasing foam cell formation. Lectin-type oxidized LDL receptor 1 (LOX-1) participates at various steps involved in the pathogenesis of atherosclerosis, and in experimental studies its blockade has been shown to affect the progression of atherosclerosis at multiple levels. In this review, we summarize the role of ox-LDL and scavenger receptors in the formation of atheroma with emphasis on effects of LOX-1 blockade.     

Oxidized LDL,LOX-1 and Atherosclerosis

An elevated level of low density lipoprotein (LDL) cholesterol constitutes a major risk factor for genesis of atherosclerosis. Ox-LDL plays a more important role in the genesis and progression of atherosclerosis than the native LDL. Ox-LDL leads to endothelial dysfunction leading to expression of adhesion molecules and recruitment of monocyte in subendothelial space. Ox-LDL is taken up by macrophages via scavenger receptors, such as SR-A1, SR-A2 and LOX-1. Lately, LOX-1, a type II membrane protein receptor of ox-LDL, has gained much importance in relation to effects of ox-LDL on endothelial biology. Endothelial cells primarily express LOX-1 as receptor for ox-LDL and ox-LDL has been shown to upregulate expression of LOX-1. In addition, ox-LDL promotes the growth and migration of smooth muscle cells, monocytes/macrophages and fibroblasts. In this review we discuss the role of ox-LDL and LOX-1 in genesis and progression of atherosclerosis.     

Enzymatically degraded LDL preferentially binds to CD14(high) CD16(+) monocytes and induces foam cell formation mediated only in part by the class B scavenger-receptor CD36

Heterogeneity of peripheral blood monocytes is characterized by specific patterns in the membrane expression of Fc gamma-receptor III (FcgammaRIII/CD16) and the lipopolysaccharide receptor (LPS receptor CD14), allowing discrimination of distinct subpopulations. The aim was to analyze the correlation of these phenotypic differences to the early interaction of freshly isolated monocytes with modified lipoproteins by the use of either enzymatically degraded low density lipoprotein (E-LDL), acetylated low density lipoprotein (ac-LDL), oxidized low density lipoprotein (ox-LDL), or native low density lipoprotein. Highest E-LDL binding was observed on CD14(high) CD16(+) monocytes as determined by flow cytometry, suggesting a selective interaction of E-LDL with distinct subpopulations of monocytes. E-LDL induced rapid foam cell formation both in predifferentiated monocyte-derived macrophages and, in contrast to ac-LDL or ox-LDL, also in freshly isolated peripheral blood monocytes. This was accompanied by upregulation of the 2 class B scavenger receptors CLA-1/SR-BI (CD36 and LIMPII Analogous-1/scavenger receptor type B class I) and CD36. Cellular binding and uptake of E-LDL was neither competed by ac-LDL nor the class A scavenger-receptor inhibitor polyinosinic acid but was partially inhibited by an excess of ox-LDL. In predifferentiated monocyte-derived macrophages, an anti-CD36 antibody inhibited cellular binding and uptake of E-LDL by approximately 20%, suggesting that recognition of these hydrolase-modified low density lipoprotein particles is mediated only in part by the class B scavenger receptor CD36.     

CD36与动脉粥样硬化

CD36是在多种组织细胞上表达的跨膜糖蛋白,属于B族清道夫受体.单核巨噬细胞上的CD36是吞噬摄取氧化型低密度脂蛋白的主要受体.除介导泡沫细胞形成外,CD36还有促进凝血和单核细胞聚集,促进炎症反应和氧化、凋亡等多种功能,其表达可被高度调控,是巨噬细胞泡沫化和动脉粥样硬化发生发展的重要因素.     

Macrophages, inflammation, and atherosclerosis

The macrophage plays a diverse array of roles in atherogenesis and lipoprotein metabolism. The macrophage functions as a scavenger cell, an immune mediator cell, and as a source of chemotactic molecules and cytokines. Chemokines have been implicated in promoting migration of monocytes into the arterial intima. Monocyte chemoattractant protein-1 (MCP-1) attracts monocytes bearing the chemokine receptor CCR-2. Macrophage expression of cyclooxygenase-2, a key enzyme in inflammation, promotes atherosclerotic lesion formation in low-density lipoprotein receptor (LDLR)-deficient mice. In the arterial intima, monocytes differentiate into macrophages, which accumulate cholesterol esters to form lipid-laden foam cells. Foam cell formation can be viewed as an imbalance in cholesterol homeostasis. The uptake of atherogenic lipoproteins is mediated by scavenger receptors, including SR-A and CD36. In the macrophage, ACAT-1 is responsible for esterifying free cholesterol with fatty acids to form cholesterol esters. Surprisingly, deficiency of macrophage ACAT-1 promotes atherosclerosis in LDLR-deficient mice. A number of proteins have been implicated in the process of promoting the efflux of free cholesterol from the macrophage, including apoE, ABCA1, and SRB-1. Macrophage-derived foam cells express the adipocyte fatty acid-binding protein (FABP), aP2, a cytoplasmic FABP that plays an important role in regulating systemic insulin resistance in the setting of obesity. ApoE-deficient mice null for macrophage aP2 expression develop significantly less atherosclerosis than controls wild type for macrophage aP2 expression. These results demonstrate a significant role for macrophage aP2 in the formation of atherosclerotic lesions independent of its role in systemic glucose and lipid metabolism. Furthermore, macrophages deficient in aP2 display alterations in inflammatory cytokine production. Through its distinct actions in adipocytes and macrophages, aP2 links features of the metabolic syndrome including insulin resistance, obesity, inflammation, and atherosclerosis.     

The process of atherogenesis — cellular and molecular interaction: from experimental animal models to humans

Atherogenesis is a disorder of the artery wall that involves: adhesion of monocytes and lymphocytes to the endothelial cell surface; migration of monocytes into the sub-endothelial space and differentiation into macrophages; ingestion of low density lipoproteins and modified or oxidised low density lipoproteins by macrophages by several pathways, including a scavenger pathway, leading to accumulation of cholesterol esters and formation of foam cells. These foam cells together with T lymphocytes form the fatty streak. Vascular smooth muscle cells migrate from the media into the intima and proliferate with the formation of atherosclerotic plaques. These processes which involve cell adhesion, migration, differentiation, proliferation and cell interaction with the extracellular matrix are regulated by a complex network/cascade of cytokines and growth regulatory peptides. Thus, atherosclerosis may be the result of a specialised chronic inflammatory fibroproliferative process which has become excessive and in its excess this protective response has become the disease state.     

Troglitazone inhibits formation of early atherosclerotic lesions in diabetic and nondiabetic low density lipoprotein receptor-deficient mice

Peroxisome proliferator-activated receptor-gamma (PPARgamma) is a ligand-activated nuclear receptor expressed in all of the major cell types found in atherosclerotic lesions: monocytes/macrophages, endothelial cells, and smooth muscle cells. In vitro, PPARgamma ligands inhibit cell proliferation and migration, 2 processes critical for vascular lesion formation. In contrast to these putative antiatherogenic activities, PPARgamma has been shown in vitro to upregulate the CD36 scavenger receptor, which could promote foam cell formation. Thus, it is unclear what impact PPARgamma activation will have on the development and progression of atherosclerosis. This issue is important because thiazolidinediones, which are ligands for PPARgamma, have recently been approved for the treatment of type 2 diabetes, a state of accelerated atherosclerosis. We report herein that the PPARgamma ligand, troglitazone, inhibited lesion formation in male low density lipoprotein receptor-deficient mice fed either a high-fat diet, which also induces type 2 diabetes, or a high-fructose diet. Troglitazone decreased the accumulation of macrophages in intimal xanthomas, consistent with our in vitro observation that troglitazone and another thiazolidinedione, rosiglitazone, inhibited monocyte chemoattractant protein-1-directed transendothelial migration of monocytes. Although troglitazone had some beneficial effects on metabolic risk factors (in particular, a reduction of insulin levels in the diabetic model), none of the systemic cardiovascular risk factors was consistently improved in either model. These observations suggest that the inhibition of early atherosclerotic lesion formation by troglitazone may result, at least in part, from direct effects of PPARgamma activation in the artery wall.     

Chronic urotensin II infusion enhances macrophage foam cell formation and atherosclerosis in apolipoprotein E-knockout mice

OBJECTIVE: Our recent studies have indicated that urotensin II, the most potent vasoconstrictor peptide identified to date, potentiates human macrophage foam cell formation and vascular smooth muscle cell proliferation, and its levels are increased in the plasma of hypertensive patients with carotid atherosclerotic plaques. In the present study, we investigated the enhancing effect of urotensin II on atherosclerosis in apolipoprotein E-knockout mice and its suppression by 4-aminoquinoline, an urotensin II receptor-selective antagonist. METHODS: Urotensin II, urotensin II + 4-aminoquinoline, or vehicle was infused for 4 weeks through an osmotic mini-pump into 9-week-old apolipoprotein E-knockout mice on a high-fat diet. Aortic atherosclerosis and foam cell formation in exudate peritoneal macrophages were examined. RESULTS: Atherosclerotic lesions as well as plasma levels of urotensin II, reactive oxygen species, and oxidized low-density lipoprotein and oxidized low-density lipoprotein-induced foam cell formation were significantly greater in urotensin II-infused mice than vehicle-infused controls. Western blotting analysis showed increased expression of scavenger receptors (CD36 and scavenger receptor class A) and acyl-CoA:cholesterol acyltransferase-1 in these macrophages. Increases in these parameters were significantly reduced by addition of 4-aminoquinoline. In apolipoprotein E-knockout mice even without urotensin II infusion, the treatment with 4-aminoquinoline for 8 weeks significantly prevented the development of atherosclerotic lesions. CONCLUSION: Our results provide the first evidence that increased plasma urotensin II level stimulates oxidized low-density lipoprotein and reactive oxygen species production and macrophage foam cell formation via increased expression of CD36, scavenger receptor class A, and acyl-CoA:cholesterol acyltransferase-1, contributing to the development of atherosclerosis in apolipoprotein E-deficient mice. Urotensin II receptor antagonism may be a promising therapeutic strategy against atherosclerosis.     

Macrophage scavenger receptor class A: A multifunctional receptor in atherosclerosis

In atherogenesis, elevated plasma levels of low density lipoprotein (LDL) lead to the chronic presence of LDL in the arterial wall. There, LDL is modified (eg, oxidized), and these modified lipoproteins activate endothelial cells, which attract circulating monocytes. These monocytes enter the vessel wall, differentiate into macrophages, and subject the modified lipoproteins to endocytosis through scavenger receptor pathways. This unrestricted uptake, which is not limited by intracellular cholesterol levels, eventually leads to the formation of lipid-filled foam cells, the initial step in atherosclerosis. Macrophage scavenger receptor class A (SRA) is thought to be one of the main receptors involved in foam cell formation, mediating the influx of lipids into the macrophages. In addition to this role in modified lipoprotein uptake by macrophages, the SRA has been shown to be important in the inflammatory response in host defense, cellular activation, adhesion, and cell-cell interaction. Given the importance of these processes in atherogenesis, these latter functions may prove to make the SRA a multifunctional player in the atherosclerotic process.     

Progression and regression of atherosclerosis in APOE3-Leiden transgenic mice: an immunohistochemical study

Apolipoprotein E3-Leiden (APOE3-Leiden) transgenic mice develop hyperlipidemia and are highly susceptible to diet-induced atherosclerosis. We have studied the progression and regression of atherosclerosis using immunohistochemistry. Female transgenic mice were fed a moderate fat diet to study atherosclerosis over a longer time period. Fatty streaks arose in the intima and consisted of lipid filled macrophages which differed in origin. All macrophages expressed the macrophage scavenger receptor while two thirds expressed sialoadhesin and were positive for an antibody recognizing marginal zone macrophages (MOMA-1). All macrophages were negative for the scavenger receptor MARCO and 50% were positive for CD4. Small fatty streaks contained CD-3 positive T-lymphocytes which were for more than 70% CD4-positive. ICAM-1 was positive both in atherosclerotic and control mice. In early plaques, fibrosis was observed on the luminal and medial site of the foam cells while smooth muscle cells were only observed in the fibrous cap. To study regression, we used a high fat, high cholesterol diet to rapidly induce atherosclerosis (14 weeks). The animals were then fed normal chow. Subsequently, atherosclerosis was assayed over time (4, 8, 16 weeks). Cholesterol levels dropped in 4 weeks to control levels.The animals did not show a significantly decrease in plaque size over time. but the percentage macrophages was significantly smaller in the animals after 4 weeks. In conclusion, the APOE3-Leiden mouse is a useful model to study the progression and regression of atherosclerosis.     

Dietary homocysteine promotes atherosclerosis in apoE-deficient mice by inducing scavenger receptors expression

Elevated plasma homocysteine (Hcy) levels have been recognized as an independent risk factor for atherosclerosis leading to cardiovascular diseases. However, the mechanisms contributing to atherosclerosis have not been delineated. Since, scavenger receptors mediated uptake of oxidized-LDL (oxLDL) by macrophages resulting in foam cell formation is an early event in atherosclerosis, we hypothesized that atherogenic effects of Hcy may be mediated via regulating expression of scavenger receptor(s). We have tested this hypothesis using apoE-/- female mice fed normal rodent chow (NC) diet or NC supplemented with Hcy in drinking water (9 g/L). Hcy-fed mice showed increased fatty streak lesions in aortic sinus/root compared to NC group without alterations in plasma lipid profiles. Similar findings were observed in the enface analysis of the descending aorta. To determine the molecular mechanisms underlying Hcy-mediated progression of fatty streak lesions, expression of scavenger receptors such as CD36 and lectin-like oxidized LDL binding protein-1 (LOX-1) in the aortic lesions were analyzed. Interestingly, Hcy-fed mice had increased immuno-positive staining for CD36 and LOX-1 in the atherosclerotic lesions compared to NC-fed mice. In vitro analyses showed neither Hcy nor HcyLDL directly affect the expression of CD36 and LOX-1 on mouse macrophages. However, Hcy supplementation in apoE-/- mice resulted in elevated oxLDL levels in plasma. Since oxLDL has been shown to upregulate the expression of CD36 and LOX-1, these findings suggest that Hcy may exert its atherogenic effect in part by elevating the levels of oxLDL. Interestingly, interaction of monocytes with Hcy-activated endothelial cells resulted in upregulation of CD36 expression on monocytes, suggesting a possible mechanism by which Hcy may upregulate CD36 expression at the lesion site. Further, these findings suggest a novel mechanism by which Hcy may promote atherogenesis.     

Vitamin E inhibits CD36 scavenger receptor expression in hypercholesterolemic rabbits

A numerous studies suggest that Vitamin E has a preventive role in atherosclerosis, although the mechanism of action still remains unclear. CD36, a member of the scavenger receptor family is centrally involved in the uptake of oxidized low density proteins (oxLDLs) from bloodstream. During the atherosclerotic process, the lipid cargo of oxLDL accumulates in macrophages and smooth muscle cells, inducing their pathological conversion to foam cells. In the present study, we investigate the role of Vitamin E on CD36 expression in an in vivo model. Atherosclerosis was induced by a 2% cholesterol containing Vitamin E poor diet. Three groups of six rabbits each were studied. The first group (control) was fed on Vitamin E poor diet. The second group was fed with Vitamin E poor diet containing 2% cholesterol and the rabbits in the third group were fed with Vitamin E poor diet containing 2% cholesterol and received injections of 50 mg/kg of Vitamin E i.m. After 4 weeks, aortas were removed and analysed by light microscopy for atherosclerotic lesions. Aortic samples were analysed for CD36 mRNA expression. The aortas of cholesterol-fed rabbits showed typical atherosclerotic lesions, detected by macroscopic and microscopic examination, and exhibited an increase in CD36 mRNA expression. Vitamin E fully prevented cholesterol induced atherosclerotic lesions and the induction of CD36 mRNA expression. The effects observed at the level of CD36 scavenger receptor expression in vivo suggest an involvement of reduced foam cell formation in the protective effect of Vitamin E against atherosclerosis.     

Oxidized low density lipoprotein-induced LFA-1-dependent adhesion and transendothelial migration of monocytes via the protein kinase C pathway

Inflammatory and immune responses are highly relevant processes in the pathogenesis of atherosclerosis, as illustrated by the central event of monocyte accumulation in atherosclerotic plaques. Integrin LFA-1-mediated adhesion of circulating monocytes to the endothelium is a prerequisite for recruitment of monocytes to these areas. Integrin-mediated adhesion is tightly regulated and integrins are only functional in response to particular monocyte activation stimuli. We investigated the role of oxidized low-density lipoprotein (LDL) in adhesion of resting monocytes prepared by elutriation from endothelium. Our results showed that: (1) oxidized LDL (and MCP-1) induced both LFA-1-mediated adhesion of monocytes to endothelial cells and transendothelial migration of monocytes; (2) oxidized LDL functionally transformed monocyte LFA-1 to an activated form; (3) oxidized LDL induced F-actin polymerization and cytoskeletal rearrangement within seconds; and (4) the LDL-associated antioxidant, -tocopherol, but not β-tocopherol, inhibited both F-actin polymerization and LFA-1-mediated adhesion of monocytes, which paralleled the effect of protein kinase C (PKC) inhibitors. Our results indicate that oxidized LDL plays a pivotal role in triggering LFA-1 activation and LFA-1-mediated adhesion and transmigration of monocytes to sites of atherosclerotic plaques, via the PKC pathway.     

腹部脂肪组织分泌抵抗素样分子α促进清道夫受体表达

目的探讨腹部脂肪组织抵抗素样分子α(RELMα)mRNA及蛋白表达情况,研究其对与动脉粥样硬化密切相关的巨噬细胞清道夫受体B(CD36)及平滑肌细胞清道夫受体A(SR-A)表达的影响。方法取C57BL/6J小鼠腹部脂肪组织,体外培养巨噬细胞及平滑肌细胞,用氧化型低密度脂蛋白(ox-LDL,ox-LDC组)以及终浓度为3×10~(-6)mmol/L(A组)、9×10~(-6)mmol/L(B组)、2.7×10~(-5)mmol/L(C组)的RELMα刺激培养细胞,对照组加等量生理盐水刺激细胞。采用RT-PCR及免疫组织化学检测脂肪细胞内RELMα表达,采用流式细胞仪检测CD36及SR-A表达。结果小鼠腹部脂肪组织可见RELMαmRNA蛋白阳性表达。与对照组比较,ox-LDL组CD36荧光强度明显增强,SR-A表达阳性率明显升高(P<0.01);与ox-LDL组比较,A、B、C组SR-A表达阳性率明显升高(P<0.05)。结论小鼠腹部脂肪组织能分泌RELMα,其不影响巨噬细胞CD36的表达,但能促进ox-LDL诱导的平滑肌细胞SR-A表达,提示腹部脂肪组织可能通过RELMα,影响SR-A表达从而促进动脉粥样硬化进展。     

单核细胞株THP-1分化为泡沫细胞过程中清道夫受体A变化及阿托伐他汀的干预作用

目的 研究单核细胞株THP-1分化为巨噬细胞、泡沫细胞过程中细胞清道夫受体A（SRA）表达、单核细胞趋化蛋白-1（MCP-1）分泌及应用阿托伐他汀干预的情况。方法 佛波醇酯诱导THP-1细胞分化为巨噬细胞,将其分为对照组、OX-LDL组（泡沫细胞组）、OX-LDL＋阿托伐他汀组（再分为低、中、高浓度3组）。用ELISA法,测定细胞培养液中MCP-1浓度。将SRA特异性结合配体DiI-Ac-LDL与细胞孵育,应用荧光显微镜观察各组细胞SRA蛋白表达及活性情况。并将MCP-1浓度与SRA蛋白活性进行相关性分析。结果400倍光镜下观察到细胞株THP-1在佛波醇酯诱导下转变为泡沫细胞。与对照组相比,OX-LDL组MCP-1表达升高,6h后升高明显（P〈0．05）,12h达高峰（P〈0．01）,24h后逐渐下降（P〈0．01）。阿托伐他汀药物干预,呈剂量依赖性降低MCP．1水平。OX-LDL组SRA蛋白活性水平明显高于对照组（P〈0．01）。阿托伐他汀干预,呈剂量依赖性下调SRA蛋白活性水平。各组细胞12hMCP．1浓度与SRA蛋白活性水平呈明显正相关（r=0．683,P〈0．01）。结论SRA、炎症因子MCP-1在THP-1细胞分化为泡沫细胞过程中发挥重要作用,阿托伐他汀抑制MCP-1与SRA表达,可能是其抗动脉粥样硬化形成的重要机制。     

白细胞介素10对人THP-1源巨噬细胞泡沫化过程中SR-A表达的影响

目的:本研究旨在观察白细胞介素-10(IL-10)对人THP-1源巨噬细胞泡沫化过程中清道夫受体A(SR-A)表达的影响,探讨在动脉粥样硬化形成中IL-10对氧化型低密度脂蛋白(ox-LDL)诱导巨噬细胞泡沫化的干预作用。方法:体外建立泡沫细胞培养体系,将细胞分为5组即THP-1单核细胞组,巨噬细胞组,IL-10刺激巨噬细胞组,ox-LDL刺激巨噬细胞组(泡沫细胞组),ox-LDL和IL-10联合刺激巨噬细胞组。采用RT-PCR和Westernbloting分别检测SR-A的mRNA和蛋白表达变化,脂质油红O化学染色方法检测各组细胞脂质摄取量的情况。结果:当THP-1分化为巨噬细胞时,SR-A开始大量表达;IL-10刺激可显著抑制巨噬细胞组SR-A的表达,其mRNA和蛋白分别下降为未刺激前的0.6倍和0.7倍,泡沫细胞形成率也下降为未刺激前的0.6倍。巨噬细胞经ox-LDL刺激形成泡沫细胞时,SR-A的表达进一步升高,其mRNA和蛋白分别增加为巨噬细胞组的1.5倍和1.4倍,泡沫细胞形成率提高为巨噬细胞组的1.7倍。在此过程中加入IL-10联合刺激,观察到SR-A的表达量有显著降低,其mRNA和蛋白均下降为单用ox-LDL刺激巨噬细胞组的0.4倍,ox-LDL的摄取量也下降为单用ox-LDL刺激巨噬细胞组的0.3倍。结论:IL-10抑制巨噬细胞SR-A表达,IL-10对ox-LDL诱导巨噬细胞SR-A的表达具明显干预作用。IL-10通过抑制SR-A表达可能在抗动脉粥样硬化的发生中发挥重要作用。