Atherosclerosis (AS) is a chronic cardiovascular disease endangering human health and is one of the most common causes of myocardial infarction and stroke. Macrophage polarization plays a vital role in regulating plaque stability. As an important component of sunlight, ultraviolet B (UVB) has been proven to promote vitamin D and nitric oxide synthesis. This research used an AS model in ApoE^−/− mice to study the effects of UVB on macrophage polarization and atherosclerotic plaque stability. In vitro, UVB irradiation increased arginase-I (Arg-I, M2 macrophage) and macrophage mannose receptor (CD206) expression, while the expression of inducible nitric oxide synthase (iNOS) (M1 macrophage) and CD86 was decreased. UVB promoted Akt phosphorylation in vitro. In vivo, UVB irradiation promoted the stabilization of atherosclerotic lesion plaques, while the phenotype of M2 macrophages increased. Our research provides new evidence for UVB in preventing and treating atherosclerosis.

动脉粥样硬化（AS）是一种危害人类健康的慢性心血管疾病，是心肌梗死和脑卒中最常见的病因之一。巨噬细胞极化在调节斑块稳定性中起着至关重要的作用。作为阳光的重要组成部分，紫外线B（UVB）已被证明可以促进维生素D和一氧化氮的合成。这项研究在 ApoE 中使用了 AS 模型^−/−小鼠研究 UVB 对巨噬细胞极化和动脉粥样硬化斑块稳定性的影响。在体外，UVB 照射增加精氨酸酶-I（Arg-I，M2 巨噬细胞）和巨噬细胞甘露糖受体 (CD206) 的表达，而诱导型一氧化氮合酶 (iNOS)（M1 巨噬细胞）和 CD86 的表达降低。UVB 在体外促进 Akt 磷酸化。在体内，UVB 照射促进动脉粥样硬化病变斑块的稳定，同时 M2 巨噬细胞的表型增加。我们的研究为 UVB 预防和治疗动脉粥样硬化提供了新的证据。