Institute of Cerebrovascular Diseases, Affiliated Hospital of Qingdao University, Qingdao 266003, China.
Clinical laboratory, Affiliated Hospital of Qingdao University, Qingdao 266003, China.
Int J Biol Macromol. 2018 Oct 15;118(Pt A):365-374. doi: 10.1016/j.ijbiomac.2018.06.054. Epub 2018 Jun 12.
Atherosclerosis (AS) is the key cause of many cardiovascular and cerebrovascular diseases. The inflammatory response and lipid metabolism disorders contribute to the development and progression of AS. This work aims to study the anti-inflammatory effect and mechanism of low molecular weight fucoidan (LMWF) obtained from Saccharina japonica on atherosclerosis in apoE-knockout mice. The experimental results showed that LMWF statistically decreased the levels of triglyceride (TRIG) and oxidative low-density lipoproteins (ox-LDL) and stabilized established atherosclerotic lesions. LMWF ameliorated the inflammatory response by down regulating IL-6 and by up regulating IL-10 transcriptional levels, and LMWF returned p-JNK and cyclin D1 to normal levels. Moreover, LMWF increased the mRNA level of CD11b in the aorta and suppressed the expression of CD11b in the intimal layer of the aorta. Therefore, LMWF prevented macrophages from developing into foam cells and prevented SMCs from migrating into the intimal layer of the aorta, which inhibited the formation of atherosclerotic plaques; and ameliorated the occurrence and development of AS.
动脉粥样硬化（AS）是许多心脑血管疾病的关键病因。炎症反应和脂质代谢紊乱促进了 AS 的发生和发展。本工作旨在研究来源于海带的低分子量褐藻糖胶（LMWF）对载脂蛋白 E 基因敲除小鼠动脉粥样硬化的抗炎作用及其机制。实验结果表明，LMWF 可统计学降低甘油三酯（TRIG）和氧化型低密度脂蛋白（ox-LDL）水平，并稳定已形成的动脉粥样硬化病变。LMWF 通过下调 IL-6 和上调 IL-10 转录水平改善炎症反应，使 p-JNK 和细胞周期蛋白 D1 恢复正常水平。此外，LMWF 增加了主动脉中 CD11b 的 mRNA 水平，并抑制了主动脉内膜层中 CD11b 的表达。因此，LMWF 阻止巨噬细胞转化为泡沫细胞，并防止平滑肌细胞向主动脉内膜层迁移，从而抑制了动脉粥样硬化斑块的形成；并改善了 AS 的发生和发展。
