| 包装 | 价格(元) |
| 1mg | 电议 |
| 5mg | 电议 |
| 10mg | 电议 |
Preparation Method | A cloned human GLP-1 receptor expressed in juvenile hamster kidney (BHK) cells was used, Study on functional assays of compounds( Liraglutide ) using SAR. |
Reaction Conditions | 10-14-10-5M liraglutide |
Applications | Liraglutide is a highly potent, long-acting GLP-1 receptor agonistand and shares 97% of its amino acid sequence identity with human GLP-1 (EC50= 61 pM). |
Cell experiment | HepG2 cell line |
Preparation Method | Cell viability assay ：HepG2 cells were seeded onto a 96-well plate, then treated with PA and LPS in the presence of liraglutide (0, 50, 100, 200, 500 nM) for 16 h. The number of viable cells was determined using Cell Counting Kit-8 (CCK-8) |
Reaction Conditions | liraglutide (0, 50, 100, 200, 500 nM) for 16 h |
Applications | The number of viable cells in hepatocytes treated with PA/LPS was significantly reduced, and liraglutide reversed the decline in cell viability in a concentration-dependent manner. Liraglutide at 100 nM significantly increased cell viability compared with higher concentrations. |
Animal models | Male ApoE KO mice on C57BL/6 background |
Preparation Method | Liraglutide (1 mg/kg) or saline was given intraperitoneally twice daily for 8 weeks (from 9th to 16th week of HFD feeding) |
Dosage form | Liraglutide (1 mg/kg) for 8 weeks |
Applications | Liraglutide treatment improved insulin sensitivity and increased Acrp30 plasma levels and transcriptional activity, Liraglutide treatment reduces liver fat content, Liraglutide was sufficient to protect mice from the inflammatory consequences of HFD and Acrp30 knockdown. |
| 产品描述 | Liraglutide is a highly potent, long-acting GLP-1 receptor agonist (EC50 = 61 pM)and shares 97% of its amino acid sequence identity with human GLP-1[6,7]. The number of viable cells in hepatocytes treated with PA/LPS was significantly reduced, and liraglutide reversed the decline in cell viability in a concentration-dependent manner. Liraglutide at 100 nM significantly increased cell viability compared with higher concentrations[1].In H9c2 cardiomyoblasts,Pretreatment with 100 nM liraglutide could efficiently inhibit TNF-α and hypoxia-induced inflammasome activation. liraglutide reversed the level of SIRT1,Liraglutide diminished the levels of ROS generation and NOX4 expression[2]. Liraglutide relieved steatosis by improving hepatic fat synthesis, transportation, storage, and use via PI3K and AMPK pathways[3].The cytoplasmic lipid droplet accumulation was visibly decreased in foam cells by treatment with liraglutide. The TG and cholesterol content in the liraglutide-treated foam cells was significantly decreased. Expression level of AMPKα1 and phosphorylated AMPKα1 was significantly increased while the expression level of SREBP1 and phosphorylated SREBP1 was significantly decreased in foam cells following treatment with liraglutide[5]. In mice,The combination of HFD, Acrp30 knockdown and ApoE deficiency had additive effects on the development of insulin resistance (IR) and NAFLD. Administration of liraglutide prevented the development of HFD and hypoadiponectinaemia-induced IR and NAFLD in this model. Liraglutide also attenuated the expression of proinflammatory cytokines or transcription factor, including TNF-α and NF-κB(65) , and the expression of two lipogenesis-related genes, Acetyl-CoA Carboxylase (ACC) and fatty acid synthase (FAS)[4]. References: |
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