1263068-83-2
1263068-83-2 結(jié)構(gòu)式
物理化學(xué)性質(zhì)
常見問題列表
IC50: 4.19? μM (TRPV4)
GSK205 (100 μM) potently antagonizes TRPV4 in 3T3-F442A adipocytes, as it effectively blocks the calcium influx caused by TRPV4 agonist.
GSK205 (5 μM; 4 days; T3-F442A adipocytes) treatment results in increases expression of thermogenic genes (Mcp1, Mip1α, Mcp3, Rantes and Vcam, et al.) and is also accompanied by a decrease in the proinflammatory gene program. This shift resembles the gene expression changes seen in TRPV4-deficient adipocytes.
RT-PCR
| Cell Line: | T3-F442A adipocytes |
| Concentration: | 5 μM |
| Incubation Time: | 4 days |
| Result: | Resulted in increased expression of thermogenic genes and is also accompanied by a decrease in the proinflammatory gene program. |
GSK205 (10 mg/kg; intraperitoneal injection; twice daily; for 7 days; for 4 weeks; male C57BL/6J mice) treatment shows significantly increases expression of thermogenic genes such as Ucp1, Pgc1a, Cidea and Cox8b. GSK205 treatment causes a reduced expression of the proinflammatory chemokines, macrophage marker and Tnfa in the EPI fat. GSK205 treatment significantly improves glucose tolerance in diet-induced obese (DIO) mice. There are no apparent sign of sickness or weight loss.
GSK205 has a relatively short half-life of 2 hours in the plasma and adipose tissues.
| Animal Model: | Male C57BL/6J mice with high-fat diet |
| Dosage: | 10 mg/kg |
| Administration: | Intraperitoneal injection; twice daily; for 7 days |
| Result: | Caused a reduced expression of the proinflammatory chemokines, macrophage marker and Tnfa in the EPI fat. Significantly improved glucose tolerance in diet-induced obese (DIO) mice. |