摘要
为探讨雅安藏茶水提物调控PPARα水平及降脂的分子机制,构建pET32a-PTD-PPARα原核重组载体,表达具有进入细胞能力的PTD-PPARα融合蛋白,利用肝细胞L02构建高脂细胞模型.SDS-PAGE和Western blotting结果显示PTD-PPARα融合蛋白纯度及特异性较高,能自由进入L02细胞并降低L02高脂细胞中脂类沉积.L02高脂细胞模型经藏茶水提物处理24 h,油红O染色表明细胞脂类沉积显著降低,Western blotting表明PPARα蛋白水平显著增加,并具有浓度梯度依赖性.结果表明:藏茶水提物可能通过促进PPARα蛋白水平抑制脂类在细胞中沉积,调控脂类代谢.
To explore the molecular mechanism of the regulation of PPARαlevel and lipid-lowering in Tibetan tea aqueous extract,the prokaryotic recombinant vector pET32a-PTD-PPAR was constructed to express PTD-PPARαfusion protein with cell-entering ability,and constructed of a high-lipid cell model using hepatocyte Lo2 cell line.SDS-PAGE and Western blotting results indicated that PTD-PPARαfusion protein had a high purity and specificity,and it could enter L02 cells and reduce lipid deposition in L02 high-fat cells.The L02 high-fat cell model was treated with Tibetan tea aqueous extract for 24 h,lipid deposition analyzed by Oil red O staining showed that cell lipid deposition was significantly decreased;western blotting also showed PPARαprotein levels increased significantly with a concentration-dependent manner.In conclusion,the results showed that the aqueous extract of Tibetan tea may inhibit the deposition of lipids in cells by regulating the level of PPARαprotein and regulate lipid metabolism.
作者
褚剑轲
曾茂
陈晓芳
李瑞
杜倩
王丹
郝军莉
CHU Jian-Ke;ZENG Mao;CHEN Xiao-Fang;LI Rui;DU Qian;WANG Dan;HAO Jun-Li(Department of Biological Sciences and Technology,Chengdu Medical College,Chengdu 610500,China)
出处
《四川大学学报(自然科学版)》
CAS
CSCD
北大核心
2019年第6期1177-1181,共5页
Journal of Sichuan University(Natural Science Edition)
基金
四川省教育厅项目(17ZA0102、16ZA0287)
四川省卫生厅项目(16PJ103
18PJ586)
国家大创项目(201513705009)
成都医学院科研创新团队项目(CYTD16-04)