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体内荧光介导断层成像显示阿托伐他汀可减少 ApoE-/- 小鼠的病变巨噬细胞。

In vivo fluorescence-mediated tomography imaging demonstrates atorvastatin-mediated reduction of lesion macrophages in ApoE-/- mice.

机构信息

Department of Anesthesiology and Intensive Care Medicine, Hannover Medical School, Hannover, Germany.

出版信息

Anesthesiology. 2013 Jul;119(1):129-41. doi: 10.1097/ALN.0b013e318291c18b.

Abstract

BACKGROUND

Macrophage recruitment into atherosclerotic plaques drives lesion progression, destabilization, and rupture. Chronic statin treatment reduces macrophage plaque content. Information on dynamics of macrophage recruitment would help assessing plaque vulnerability and guiding therapy. Techniques to image macrophage homing to vulnerable plaques in vivo are scarcely available. The authors tested if noninvasive fluorescence-mediated tomography (FMT) can assess plaque-stabilizing effects of short-term high-dosage atorvastatin.

METHODS

Macrophages from green-fluorescent-protein-transgenic mice were labeled with a near-infrared fluorescent dye and were injected IV in apolipoprotein E-deficient mice (n=9) on Western diet 7 days after guidewire-injury of the carotid artery. FMT-scans, 2 and 7 days thereafter, quantified macrophage recruitment into carotid artery plaques. Atorvastatin was tested for macrophage adhesion, proliferation, and viability (n=5 to 6) in vitro. Fourteen mice received atorvastatin or vehicle for 4 days after 16 weeks on Western diet. FMT assessed macrophage recruitment into aortic and innominate artery lesions. Means (±SD)% are reported.

RESULTS

Double-labeled macrophages were recruited into carotid artery lesions. FMT resolved fluorescence projecting on the injured carotid artery and detected a signal increase to 300% (±191) after guidewire injury. Atorvastatin reduced macrophage adhesion to activated endothelial cells by 36% (±19). In a clinically relevant proof-of-concept intervention, FMT-imaging detected that 4 days atorvastatin treatment reduced macrophage recruitment by 57% (±8) indicating plaque stabilization. Immunohistochemistry confirmed reduced macrophage infiltration.

CONCLUSIONS

FMT optical imaging proved its high potential for clinical applicability for tracking recruitment of near-infrared fluorescent-labeled macrophages to vulnerable plaques in vivo. FMT-based quantification of macrophage recruitment demonstrated rapid plaque stabilization by 4-day atorvastatin treatment in apolipoprotein E-deficient mice.

摘要

背景

巨噬细胞募集进入动脉粥样硬化斑块会驱动病变进展、不稳定和破裂。慢性他汀类药物治疗可减少巨噬细胞斑块含量。有关巨噬细胞募集动力学的信息将有助于评估斑块的脆弱性并指导治疗。目前很少有技术可用于在体内成像易损斑块中的巨噬细胞归巢。作者测试了非侵入性荧光介导断层扫描(FMT)是否可以评估短期高剂量阿托伐他汀对斑块稳定的作用。

方法

用近红外荧光染料对绿色荧光蛋白转基因小鼠的巨噬细胞进行标记,在载脂蛋白 E 缺陷小鼠(n=9)接受颈动脉导丝损伤后第 7 天经静脉注射。FMT 扫描在 2 天和 7 天后定量测量巨噬细胞募集到颈动脉斑块中的情况。阿托伐他汀在体外测试对巨噬细胞黏附、增殖和活力的影响(n=5 至 6)。14 只小鼠在接受西方饮食 16 周后再接受阿托伐他汀或载体治疗 4 天。FMT 评估了主动脉和无名动脉病变中巨噬细胞的募集情况。报告均值(±SD)%。

结果

双标记的巨噬细胞被募集到颈动脉病变中。FMT 解析了对损伤的颈动脉的荧光投射,并在导丝损伤后检测到信号增加 300%(±191)。阿托伐他汀可使巨噬细胞黏附到活化的内皮细胞减少 36%(±19)。在具有临床意义的概念验证干预中,FMT 成像检测到 4 天阿托伐他汀治疗可使巨噬细胞募集减少 57%(±8),表明斑块稳定。免疫组织化学证实了巨噬细胞浸润的减少。

结论

FMT 光学成像证明了其在临床应用中的高潜力,可用于在体内跟踪近红外荧光标记的巨噬细胞向易损斑块的募集。基于 FMT 的巨噬细胞募集定量分析表明,在载脂蛋白 E 缺陷小鼠中,阿托伐他汀治疗 4 天可迅速稳定斑块。

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