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| 1 | 咖啡酸苯乙酯对HepG2细胞氧化应激和脂质代谢的调节作用显示文摘咖啡酸苯乙酯(caffeic acid phenethyl ester,CAPE)是来源于蜂胶中的一种天然多酚物质,具有良好的调节脂代谢生物活性,但其调节脂代谢的分子机制尚不明确,本研究利用CAPE处理油酸诱导的人肝脏肿瘤细胞HepG2,通过转录组学探讨其在细胞水平上改善脂代谢的作用与机制。结果表明,与高脂肪组相比,经过CAPE干预后的细胞脂质积累情况得到明显的改善,转录组水平上共筛选出3270个差异表达基因(differentially expressed genes,DEGs),其中表达上调的DEGs有1351个,表达下调的DEGs有1919个。经京都基因与基因组百科全书(Kyoto Encyclopedia of Genes and Genomes,KEGG)功能注释分析发现,CAPE处理后的DEGs显著注释到脂质代谢相关通路上。由KEGG信号通路富集分析显示,富集较显著的信号通路为HIF-1α通路和脂肪酸分解代谢通路,其中CAPE组HIF-1α、PPARα、CPT1A、FABP5等基因表达水平比高脂肪组分别提高了0.326、0.661、1.039、1.598倍。综上,CAPE可能通过HIF-1α通路改善高脂细胞氧化应激,并通过PPARα和脂肪酸氧化分解途径改善高脂诱导细胞的脂代谢紊乱。本实验可为CAPE调节脂代谢的分子机制及调节高脂膳食脂代谢紊乱的深入研究提供一定的理论参考。 | 刘畅 常超 陈瑞达 林萌慧 孙蓉 蔡成岗 赵敏洁 蔡海莺 | 2023 | 食品科学2023，44，17： | 1 |
| 2 | SREBP/PCSK9通路与抗精神病药物所致脂代谢紊乱相关性的研究进展显示文摘抗精神病药物是治疗精神分裂症的主要药物,但其使用会导致脂代谢紊乱,从而增加患者发生心血管疾病的风险,缩短患者的预期寿命,并严重影响治疗的依从性。目前,抗精神病药物引起脂代谢紊乱的具体机制尚不清楚。固醇调节元件结合蛋白(sterol regulatory element binding protein,SREBP)是调控脂代谢的关键转录因子。前蛋白转化酶枯草溶菌素9(proprotein convertase subtilisin/kexin type 9,PCSK9)作为SREBP下游调控基因之一,对低密度脂蛋白胆固醇(low density lipoprotein cholesterol,LDL-C)具有重要的调控作用,是最近降脂药物研究的重要靶点。近期研究表明,抗精神病药物可以通过SREBP/PCSK9通路影响脂代谢。深入了解该通路在抗精神药物相关代谢异常中的作用机制将促进精神分裂症患者脂代谢紊乱的预防和新药的研发应用。 | 马家树 郑云哨 孙丰霞 樊运莉 范允明 苏现彪 王忠宝 翁柠 李然然 | 2023 | 中南大学学报(医学版)2023，48，10： | 0 |
| 3 | Sortilin-induced lipid accumulation and atherogenesis are suppressed by HNF1b SUMOylation promoted by flavone of Polygonatum odoratum显示文摘This study aims to investigate the impact of hepatocyte nuclear factor 1β(HNF1b)on macrophage sortilin-mediated lipid metabolism and aortic atherosclerosis and explore the role of the flavone of Polygonatum odoratum(PAOA-flavone)-promoted small ubiquitin-related modifier(SUMO)modification in the atheroprotective efficacy of HNF1b.HNF1b was predicted to be a transcriptional regulator of sortilin expression via bioinformatics,dual-luciferase reporter gene assay,and chromatin immunoprecipitation.HNF1b overexpression decreased sortilin expression and cellular lipid contents in THP-1 macrophages,leading to a depression in atherosclerotic plaque formation in low-density lipoprotein(LDL)receptor-deficient(LDLR−/−)mice.Multiple SUMO1-modified sites were identified on the HNF1b protein and co-immunoprecipitation confirmed its SUMO1 modification.The SUMOylation of HNF1b protein enhanced the HNF1b-inhibited effect on sortilin expression and reduced lipid contents in macrophages.PAOA-flavone treatment promoted SUMO-activating enzyme subunit 1(SAE1)expression and SAE1-catalyzed SUMOylation of the HNF1b protein,which prevented sortilin-mediated lipid accumulation in macrophages and the formation of atherosclerotic plaques in apolipoprotein E-deficient(ApoE−/−)mice.Interference with SAE1 abrogated the improvement in lipid metabolism in macrophage cells and atheroprotective efficacy in vivo upon PAOA-flavone administration.In summary,HNF1b transcriptionally suppressed sortilin expression and macrophage lipid accumulation to inhibit aortic lipid deposition and the development of atherosclerosis.This anti-atherosclerotic effect was enhanced by PAOA-flavone-facilitated,SAE1-catalyzed SUMOylation of the HNF1b protein. | Fang LIU Shirui CHEN Xinyue MING Huijuan LI Zhaoming ZENG Yuncheng LV | 2023 | Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)2023，24，11： | 0 |
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