香菇多糖
机制(生物学)
高脂血症
对接(动物)
化学
药理学
分子动力学
计算生物学
生物化学
医学
计算化学
生物
内分泌学
物理
多糖
护理部
量子力学
糖尿病
作者
Zhongxing Chu,Linna Zeng,Feiyan Yang,Zuomin Hu,Yi Luo,Yaping Zhou,Yiping Tang,Feijun Luo
标识
DOI:10.1016/j.fbio.2024.104306
摘要
Hyperlipidemia is closely related to multiple diseases and is characterized by abnormal serum lipid profiles. The biological function of lentinan in mice and rats was studied, but the mechanism of its lipid-lowering effect was not completely clear. In this study, network pharmacological analysis, molecular docking, and molecular dynamics simulation were used to explore the potential mechanism of its lipid-lowering effect and high-fat diet (HFD) mice was used to confirm the predicted mechanism. Our results indicated that lentinan could ameliorate hyperlipidemia by regulating peroxisome proliferator-activated receptors (PPARs), sterol response element-binding protein-1 (SREBP1), and nuclear factor kappa-B (NF-κB) in the hepatic tissues of mices. Further animal experiment showed that lentinan could regulate the mRNA expressions of lipid metabolism-related genes, such as PPARα, PPARδ, PPARγ, cluster of differentiation 36 (CD36) and SREBP-1c. Moreover, lentinan supplementation could reduce the expressions of inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and inducible nitric oxide sythase (iNOS). In cell model, lentinan also could inhibit oleic acid-induced lipid droplet formation and the expressions of lipid metabolism-related genes and reduced inflammatory factor expressions in HepG2 cells, which further approved the results of animal experiment. Taken together, our results suggest that lentinan can ameliorate hyperlipidemia via regulating lipid metabolism-related gene expressions and reduce obesity-induced inflammatory response.
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