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海带多糖通过抑制血管平滑肌细胞向成骨细胞分化来抑制血管钙化。

Laminaria japonica Polysaccharide Inhibits Vascular Calcification via Preventing Osteoblastic Differentiation of Vascular Smooth Muscle Cells.

作者信息

Li Xue-Ying, Li Qiang-Ming, Fang Qing, Zha Xue-Qiang, Pan Li-Hua, Luo Jian-Ping

机构信息

School of Biological and Medical Engineering, Hefei University of Technology , Hefei 230009, People's Republic of China.

School of Food Science and Engineering, Hefei University of Technology , Hefei 230009, People's Republic of China.

出版信息

J Agric Food Chem. 2018 Feb 28;66(8):1821-1827. doi: 10.1021/acs.jafc.7b06115. Epub 2018 Feb 16.

Abstract

This study aimed to investigate the effect and underlying mechanism of a purified Laminaria japonica polysaccharide (LJP61A) on preventing vascular calcification (VC). In the adenine-induced chronic renal failure (CRF) mice VC model and the β-glycerophosphate (β-GP)-induced vascular smooth muscle cells (VSMC) calcification model, LJP61A was found to significantly inhibit VC phenotypes as determined by biochemical analysis and von Kossa, alizarin red, and immunohistochemical staining. Meanwhile, LJP61A remarkably up-regulated the mRNA levels of VSMC related markers and down-regulated the mRNA levels of sodium-dependent phosphate cotransporter Pit-1. In addition, LJP61A could significantly decrease the protein levels of core-binding factor-1, osteocalcin, bone morphogenetic protein 2, and receptor activator for nuclear factor-κB ligand, and it can increase the protein levels of osteoprotegerin and matrix gla protein. These results indicated that LJP61A ameliorated VC both in vivo and in vitro via preventing osteoblastic differentiation of VSMC, suggesting LJP61A might be a potential therapeutic agent for VC in CRF patients.

摘要

本研究旨在探讨纯化的海带多糖(LJP61A)对预防血管钙化(VC)的作用及其潜在机制。在腺嘌呤诱导的慢性肾衰竭(CRF)小鼠VC模型和β-甘油磷酸酯(β-GP)诱导的血管平滑肌细胞(VSMC)钙化模型中,通过生化分析、冯科萨染色、茜素红染色和免疫组化染色发现,LJP61A能显著抑制VC表型。同时,LJP61A显著上调VSMC相关标志物的mRNA水平,并下调钠依赖性磷酸盐共转运蛋白Pit-1的mRNA水平。此外,LJP61A可显著降低核心结合因子-1、骨钙素、骨形态发生蛋白2和核因子κB受体激活剂配体的蛋白水平,并可提高骨保护素和基质γ-羧基谷氨酸蛋白的蛋白水平。这些结果表明,LJP61A通过阻止VSMC向成骨细胞分化在体内和体外均改善了VC,提示LJP61A可能是CRF患者VC的潜在治疗药物。

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