Filipek Agnieszka, Sadowska Agnieszka, Skłodowska Monika, Muskała Maja, Czepielewska Edyta
Chair and Department of Pharmaceutical Biology, Medical University of Warsaw, Banacha 1, 02-097 Warsaw, Poland.
School of Health and Medical Sciences, Vizja University, Okopowa 59, 01-043 Warsaw, Poland.
Int J Mol Sci. 2025 Jul 4;26(13):6444. doi: 10.3390/ijms26136444.
Syringin is a phenylpropanoid glycoside isolated from the bark of . Phillygenin is a lignan obtained mainly from the fruits and flowers of . Both compounds have shown potent anti-inflammatory and antioxidant properties. We investigated the potential role of syringin and phillygenin in preventing lipid deposition in macrophages. Syringin and phillygenin significantly ( < 0.001) reduced lipid deposition in macrophages in a dose-dependent manner. For syringin, the greatest reduction in CD36 receptor expression was found to be over 80% (50 μg/mL) compared to the cholesterol-stimulated control ( < 0.001). Phillygenin inhibited CD36 receptor expression by approximately 25% (50 μg/mL), compared to the stimulated control ( < 0.05). For syringin, the CD36 receptor regulation pathway was PPAR-γ dependent. Phillygenin showed a statistically significant ( < 0.001) increase in the expression of the ABCA1 transporter: 2.5-fold (10 μg/mL), 3-fold (20 μg/mL) and 4-fold (50 μg/mL) compared to the cholesterol-stimulated control. Syringin did not significantly increase ABCA1 expression. For phillygenin, the activation pathway of the ABCA1 transporter was HO-1dependent. Our study showed that syringin inhibits the cholesterol-induced differentiation of macrophages into foam cells. Moreover, phillygenin increased cholesterol efflux from macrophages. Therefore, syringin and phillygenin may be valuable agents in the prevention of early and late atherosclerosis.
紫丁香苷是从[植物名称]树皮中分离出的一种苯丙素苷。连翘酯苷是一种主要从[植物名称]的果实和花中获得的木脂素。这两种化合物均显示出强大的抗炎和抗氧化特性。我们研究了紫丁香苷和连翘酯苷在预防巨噬细胞脂质沉积中的潜在作用。紫丁香苷和连翘酯苷均以剂量依赖性方式显著（<0.001）降低了巨噬细胞中的脂质沉积。对于紫丁香苷，与胆固醇刺激的对照组相比，发现CD36受体表达的最大降低超过80%（50μg/mL）（<0.001）。与刺激对照组相比，连翘酯苷在50μg/mL时抑制CD36受体表达约25%（<0.05）。对于紫丁香苷，CD36受体调节途径是PPAR-γ依赖性的。连翘酯苷显示ABCA1转运蛋白的表达有统计学显著增加（<0.001）：与胆固醇刺激的对照组相比，分别为2.5倍（10μg/mL）、3倍（20μg/mL）和4倍（50μg/mL）。紫丁香苷未显著增加ABCA1表达。对于连翘酯苷，ABCA1转运蛋白的激活途径是HO-1依赖性的。我们的研究表明，紫丁香苷抑制胆固醇诱导的巨噬细胞分化为泡沫细胞。此外，连翘酯苷增加了巨噬细胞的胆固醇外流。因此，紫丁香苷和连翘酯苷可能是预防早期和晚期动脉粥样硬化的有价值药物。
